 |
|
Here is an excellent example how lessening the level of inflammation directly lessens the intensity of a disease. Below is a scientific study that was done for ALS (Lou Gehrig's Disease). It's a horrible disease the has baffled scientists for years. A few years ago scientists discovered that inflammation was a factor in ALS. As you will see, an anti-inflammatory treatment helped to lessen the effect of the disease. (It's crucial to remember that when it comes to healing inflammation, the hands of the scientific community are tied. There are no anti-inflammatory drugs (NSAIDs) on the market that don't create harmful side-effects with prolonged use).
On this page you will find scientific evidence showing that Acne Acromegaly Aging Alzheimer's Amyloidosis Amyotrophic Lateral Sclerosis (ALS) Anemia Aortic Valve Stenosis Arthritis Asthma Ataxia Attention Deficit Hyperactivity Disorder (ADHD) Cancer Celiac Disease Chronic Fatigue Syndrome Chronic Obstructive Pulmonary Disease Chronic Sarcoidosis Chronic Venous Disorder Colitis Crohn's Disease Cryoglobulinemia Cystic Fibrosis Depression Diabetes Erectile Dysfunction (ED) Fibromyalgia Heart Disease Hodgkin Disease Human Immunodeficiency Virus (HIV) Huntington's disease Irritable Bowel Syndrome Kidney Disease / Renal Failure Liver Disease Lupus Lyme Disease Migraines Multiple Sclerosis Narcolepsy Neuropathy Obesity Pancreatitis Parkinson's Poliomyelitis (Polio) Pregnancy Psoriasis Pulmonary Hypertension Scleroderma Sjogren's Syndrome Sleep Apnea Small Intestinal Bacterial Overgrowth (SIBO) Spinal Cord Conditions Stroke Tourette's Syndrome Tuberculosis are ALL directly linked to inflammation. 
What do heart disease, stroke, diabetes, Alzheimer's disease, Parkinson's disease, arthritis, allergies, asthma, gout and irritable bowel syndrome have in common? These and many other common health conditions are all associated with inflammation. Other diseases include MS, Osteoporosis, Obesity, Allergies including Asthma and Food Intolerances, Chronic Fatigue Syndrome and Fibromyalgia. Inflammation is now being recognized as the common link that may explain the association between otherwise distinct conditions. For example, did you know that there was an association between asthma and irritable bowel syndrome, or heart attack and dental problems, or gout and heart disease, or allergies and diabetes? It is now getting clearer that these conditions are related by the presence of inflammation. Leading researchers in completely different areas of medicine have independently and repeatedly come to the same conclusion; that inflammation plays a key role in the development of a variety of seemingly unrelated illnesses. For example, in 1997, researchers in neurology discovered an interesting finding, that is, that people who had been taking anti-inflammatory medications such as Ibuprofen seemed to have much lower rates of Alzheimer's disease than the general population. They published their findings in the journal Neurology. A second study published in the New England Journal of Medicine November 22, 2001 also showed an 80% reduction in the risk of Alzheimer's disease in people taking some anti-inflammatory medicinces daily for two years. It has been demonstrated that depression can be reduced with high-dose fish oil supplementation, as well as the disability caused by multiple sclerosis. For example, a decrease of the AA/EPA ratio from 6 to 1.5 in multiple sclerosis patients was associated with a 90-percent reduction in acute attacks and a 25-percent decrease in overall disability after two years. Other studies have indicated that an elevated AA/EPA ratio is strongly associated with the severity of depression. Recent studies have indicated that children with ADHD have high AA/EPA ratios, and when those AA/EPA ratios are lowered to the level found in the Japanese population, then significant behavioral improvements were observed.
"Effect of dietary advice and n-3 supplementation in newly diagnosed MS patients." Nordvik I, Myhr K-M, Nyland H, and Bjerve KS. Act Neurol Scand 102: 143-149 (2000) "Fatty acid composition in major depression: decreased n-3 fractions in cholesterol esters and increased C20:4n6/C20:5n3 ratio in cholesterol ester and phospholipids." Maes M. J Affect Dis 38: 35-46 (1996) "Arachidonic acid to eicosapentaenoic acid ratio in blood samples correlates positively with clinical symptoms of depression." Adams P, Lawson S, Sanigorski A, and Sinclair AJ. Lipids 31: S157-S161 (1996) UltraPrevention, www.ultraprevention.com/prevention/heat.htm A Huge Number of Illnesses are Caused by Inflammation, Alex Howard, NaturalNews.com, October 27, 2009 www.naturalnews.com/027335_inflammation_health_immune_system.html Aging and Inflammation, LifeExtention.com www.lef.org/protocols/prtcl-146.shtml "Definition of itis." MedicineNet, www.medterms.com/script/main/art.asparticlekey=4061 
Acne vulgaris affects as much as 80% of the adolescent population and persists in approximately 3% of middle-aged adults. Only a percentage of these persons seek medical help, however, acne can cause levels of anxiety and depression akin to a chronic illness. A recurring question from patients who seek help from various healthcare professionals - their pharmacist, family doctor or dermatologist, is "why?" They also ask questions about a possible familial link, the impact of their diet and the association with their hormones. The following review aims to link these factors with the end result - inflammation. "Pathways to inflammation: acne pathophysiology." Taylor M, Gonzalez M, Porter R. Eur J Dermatol. 2011 May 20. Acne vulgaris is a skin disease affecting pilosebaceous glands in which Propionibacterium acnes (P. acnes) induced inflammation plays a central role. In order to develop new therapies against the inflammatory events, we evaluated the modulating effect of a new undecyl-rhamnoside, APRC11, on different markers of the inflammation. In conclusion, the new undecyl-rhamnoside APRC11 is able to down-regulate the expression of molecules implicated in cutaneous inflammation and whose expression is induced by P. acnes, confirming its potential interest in inflammatory acne. "Anti-inflammatory properties of a new undecyl-rhamnoside (APRC11) against P. acnes." Isard O, Lvque M, Knol AC, Aris MF, Khammari A, Nguyen JM, Castex-Rizzi N, Drno B. Arch Dermatol Res. 2011 Apr 3. 
Active acromegaly is associated with increased mortality from cardiovascular causes. Several studies have shown increased atherogenic risk factors and biomarkers of inflammation and atherosclerosis in association with growth hormone excess. The aim of this study was to evaluate oxidized low density lipoprotein (oxLDL) levels and some modulators of LDL oxidative modification in patients with acromegaly. "Increased oxidized low density lipoprotein associated with high ceruloplasmin activity in patients with active acromegaly." Boero L, Cuniberti L, Magnani N, Manavela M, Yapur V, Bustos M, Rosso LG, Meroo T, Marziali L, Viale L, Evelson P, Negri G, Brites F. Clin Endocrinol (Oxf). 2010 May;72(5):654-60. Epub 2009 Aug 4. Serum tumour necrosis factor-alpha and interleukin-8 levels in acromegalic patients: acromegaly may be associated with moderate inflammation. "Serum tumour necrosis factor-alpha and interleukin-8 levels in acromegalic patients: acromegaly may be associated with moderate inflammation." Arikan S, Bahceci M, Tuzcu A, Gokalp D. Clin Endocrinol (Oxf). 2009 Mar;70(3):498-9. Epub 2008 Jul 31. Nicotinamide phosphoribosyltransferase (NAMPT)/PBEF/visfatin is a widely expressed cytokine with various effects on glucose and lipid metabolism, cell survival, and inflammation. Despite a favorable body composition profile, acromegalic patients present insulin resistance, increased cardiovascular risk, and higher incidence of secondary tumors. "Adipocytes as a source of increased circulating levels of NAMPT/visfatin in active acromegaly." C Olarescu, T Ueland, T Lekva, T B Dahl, P Aukrust, B Halvorsen & J Bollerslev. Endocrine Abstracts (2011) 26 P192 
Although inflammatory responses in the brain have been recognised for years as critical in neurodegeneration and behaviour in a number of neurological and psychiatric disorders, their role for the development, treatment and prevention of ADHD has been so far largely overlooked, although historically, ADHD symptoms were initially observed in patients who survived an ONJ infection, i.e. inflammation. In this review, we discuss the interrelationship between different ADHD risk factors and inflammation with respect to the triggered molecular mechanisms and the contribution they are likely to have to this disorder. "Inflammation: good or bad for ADHD" Donev R, Thome J. Atten Defic Hyperact Disord. 2010 Dec;2(4):257-66. Epub 2010 Nov 10. We propose that obesity and ADHD represent different manifestations of the same underlying dysfunction, a phenomenon we term environmental oversampling syndrome. The emerging association between psychiatric and metabolic disorders suggests a fundamental biologic link between these two systems. In addition, the immune system may represent yet another form of intelligence. The designation of syndrome X subsumes seemingly unrelated metabolic and inflammatory entities. Environmental oversampling syndrome may represent an even more inclusive concept that encompasses various metabolic, inflammatory, and behavioral conditions. Apparently disparate conditions such as insulin resistance, diabetes, hypertension, syndrome X, obesity, ADHD, depression, psychosis, sleep apnea, inflammation, autism, and schizophrenia may operate through common pathways, and treatments used exclusively for one of these conditions may prove beneficial for the others. Obesity and ADHD may represent different manifestations of a common environmental oversampling syndrome: a model for revealing mechanistic overlap among cognitive, metabolic, and inflammatory disorders." Bazar KA, Yun AJ, Lee PY, Daniel SM, Doux JD. Med Hypotheses. 2006;66(2):263-9. Attention deficit-hyperactivity disorder (ADHD) is a prevalent childhood neuropsychiatric disorder, characterized by age-inappropriate and impairing levels of inattention, hyperactivity and impulsiveness. Approximately 5-10% of school-age children are affected by ADHD, and in many cases, symptoms persist into adolescence and adulthood. Cytokines are key mediators of immune function and can be either pro-inflammatory or anti-inflammatory. Recently few studies have suggested involvement of cytokine pathways in subjects with ADHD. Polymorphism of IL-1 receptors antagonists' alleles have been suggested in families and subjects suffering from ADHD. Moreover, a new variant of inflammatory bowel disease, another immunological based disease, was recently suggested in children with ADHD and other developmental disorders. There are no other published reports on cytokine production in children who suffer from ADHD. "Inflammation in Children With Attention-Deficit/Hyperactivity Disorder." Nachum Vaisman, Prof. (MD) Tel-Aviv Sourasky Medical Center. (2007) ClinicalTrials.gov Identifier: NCT00391495 
Our objective is to determine the association among aging, inflammation, and cytokine production by peripheral blood mononuclear cells. We examined production of interleukin-1 ( (IL-1 ), tumor necrosis factor- (TNF-), IL-1 receptor antagonist (IL-IRa), and IL-6 in 711 elderly participants in the Framingham Heart Study (mean age, 79 y) and 21 young healthy volunteers (mean age, 39 y). The elderly subjects were categorized by serum C-reactive protein (CRP) concentration, a marker of systemic inflammation. Production of IL-6 (p < .00001) and IL-1Ra(p < .00001) was higher in the elderly subjects than in the control group. IL-6 production increased with increasing CRP, whereas IL-1RA was uniformly elevated in elderly subjects regardless of CRP. Although limited by the small control group, these data suggest that dysregulation of some inflammatory cytokines occurs with age, but the role of inflammation in aging remains unclear. "Monocyte Cytokine Production in an Elderly Population: Effect of Age and Inflammation." Ronenn Roubenoff, Tamara B. Harris, Leslie W. Abad, Peter W. F. Wilson, Gerard E. Dallal and Charles A. Dinarello. J Gerontol A Biol Sci Med Sci (1998) 53A (1): M20-M26. doi: 10.1093/gerona/53A.1.M20 Commonalities between the effects of aging and those observed with diabetes, including visual impairment, vascular dysfunction, and increased inflammatory response, have led to the hypothesis that diabetes-associated pathologies reflect an "advanced aging" phenotype. The commonalities in retinal age-related and diabetes-induced molecular alterations provide support for the hypothesis that diabetes and aging engage some common para-inflammatory processes. "Age-related alterations in retinal neurovascular and inflammatory transcripts." Van Kirk CA, Vanguilder HD, Young M, Farley JA, Sonntag WE, Freeman WM. Mol Vis. 2011;17:1261-74. Epub 2011 May 7. Neuropsychiatric symptoms are common complaints of elderly persons. Recent data suggest that chronic low-grade inflammation, a fundamental characteristic of aging, plays a role. Our findings show that chronic low-grade inflammation in aging is associated with alterations in enzymatic pathways involved in monoamine metabolism and suggest that these alterations might participate in the pathophysiology of neuropsychiatric symptoms in elderly persons. "Chronic Low-Grade Inflammation in Elderly Persons Is Associated with Altered Tryptophan and Tyrosine Metabolism: Role in Neuropsychiatric Symptoms." Capuron L, Schroecksnadel S, Fart C, Aubert A, Higueret D, Barberger-Gateau P, Lay S, Fuchs D. Biol Psychiatry. 2011 Jan 28. Aging results in an increase of inflammatory cytokines (destructive cell-signaling chemicals) that contribute to the progression of many degenerative diseases (Van der Meide et al. 1996; Licinio et al. 1999). Rheumatoid arthritis is a classic autoimmune disorder in which excess levels of cytokines such as tumor necrosis factor-alpha (TNF-a), interleukin-6 (IL-6), interleukin 1b [IL-1(b)], and/or interleukin-8 (IL-8) are known to cause or contribute to the inflammatory syndrome (Deon et al. 2001). Eating high temperature cooked food is another contributor in the production of inflammatory cytokines. In fact, it has been shown that eating high temperature cooked food leads to the formation of advanced glycation end (AGE) products. Glycation can be described as the binding of a protein molecule to a glucose molecule resulting in the formation of damaged protein structures. Many age-related diseases such as arterial stiffening, cataract and neurological impairment are at least partially attributable to glycation. These destructive glycation reactions render proteins in the body cross-linked and barely functional. As these degraded proteins accumulate, they cause cells to emit signals that induce the production of inflammatory cytokines. The glycation process is presently irreversible, though an important study indicates a drug in clinical trials may be partially effective. According to a Proceedings of the National Academy of Sciences study, consuming foods cooked at high temperature accelerates the glycation process, and the subsequent formation of advanced glycation end products. Aging and Inflammation, LifeExtention.com www.lef.org/protocols/prtcl-146.shtml We explored whether gliadin antibody(AGA)-positivity without tissue transglutaminase antibodies (tTGA) is persistent in the elderly population and whether such positivity indicates overt or potential coeliac disease in genetically predisposed individuals. AGA-positivity was persistent in 81% of those initially positive. Amongst the 49 clinically studied and 36 endoscopied cases only one (2.8%) had coeliac disease. Many (54%) showed signs of inflammation in the biopsy, without villous atrophy. "Persistently positive gliadin antibodies without transglutaminase antibodies in the elderly: Gluten intolerance beyond coeliac disease." Ruuskanen A, Luostarinen L, Collin P, Krekel I, Patrikainen H, Tillonen J, Laurila K, Haimila K, Partanen J, Mki M, Valve R, Kaukinen K. Dig Liver Dis. 2011 Jun 3. 
Studies increasingly indicate that inflammation induced by B-amyloid (AB) contributes to the progression of Alzheimer's disease (AD). How to inhibit the enhanced production of proinflammatory cytokines stimulated by AB is an important research subject for the treatment of AD. "Lipoxin A(4) inhibits the production of proinflammatory cytokines induced by -amyloid in vitro and in vivo." Wu J, Wang A, Min Z, Xiong Y, Yan Q, Zhang J, Xu J, Zhang S. Biochem Biophys Res Commun. 2011 May 13;408(3):382-7. Epub 2011 Apr 8. Our study shows that infection-induced acute or chronic inflammation significantly exacerbates tau pathological characteristics, with chronic inflammation leading to impairments in spatial memory. During chronic inflammation, we found that inhibiting glycogen synthase kinase-3beta activity with lithium reduced tau phosphorylation and the accumulation of insoluble tau and reversed memory impairments. Taken together, infectious agents that trigger central nervous system inflammation may serve as a comorbidity for AD, leading to cognitive impairments by a mechanism that involves exacerbation of tau pathological characteristics. "Inflammation Induced by Infection Potentiates Tau Pathological Features in Transgenic Mice." Sy M, Kitazawa M, Medeiros R, Whitman L, Cheng D, Lane TE, Laferla FM. Am J Pathol. 2011 Apr 29. B-amyloid 1-42 (AB1-42)-induced learning and memory impairment in rats is believed to be associated with inflammation. Cytokine production is a key pathologic event in the progression of inflammatory processes. In this rat study, soybean isoflavones (SIF) was used to investigate it's protective effects on inflammation caused by B-amyloid 1-42 (AB1-42), which is associated with learning and memory impairment in Alzheimer disease. Our results suggested that SIF reduced the cytokine cascade and inflammatory response induced by AB1-42 which could result in the improvement of spatial learning and memory ability impairment in the rats. "Soybean isoflavone alleviates B-amyloid 1-42 induced inflammatory response to improve learning and memory ability by down regulation of Toll-like receptor 4 expression and nuclear factor-B activity in rats." Ding BJ, Ma WW, He LL, Zhou X, Yuan LH, Yu HL, Feng JF, Xiao R. Int J Dev Neurosci. 2011 Apr 14. Activated microglial cells, which are the resident macrophages of the central nervous system, surround amyloid beta-plaques in Alzheimer's disease (AD) brains. Inflammation including microglial activation may contribute in AD pathogenesis, and biomarkers for this process may thus be of value to study AD pathogenesis and might facilitate development of therapies targeting these cells. "Cerebrospinal Fluid Microglial Markers in Alzheimer's Disease: Elevated Chitotriosidase Activity but Lack of Diagnostic Utility." Mattsson N, Tabatabaei S, Johansson P, Hansson O, Andreasson U, Mansson JE, Johansson JO, Olsson B, Wallin A, Svensson J, Blennow K, Zetterberg H. Neuromolecular Med. 2011 May 13. Allergists and immunologists aren't the only medical specialists interested in inflammation these days. In the journal Neurology in 1997, neurologists presented research that people who had been regularly taking anti-inflammatory medicine like Ibuprofen had much lower rates of Alzheimer's disease. In the New England Journal of Medicine in 2001, a study showed an 80% reduction in risk of Alzheimer's among those taking anti-inflammatory medicines daily for two years. Linda Van Eldik, neurobiologist at Northwestern University School of Medicine, explains that whenever the brain is injured or irritated, glial cells pump out cytokines, chemical signals to begin the inflammatory process. However, "in chronic neurodegenerative diseases like Alzheimer's, these glial cells are actived too high or too long or both," says Van Eldik. "Chronic Inflammation & Chronic Disease" Allergy Consumer Report, Volume Four, Issue Two, February 2007 
Renal amyloidosis is a detrimental disease caused by the deposition of amyloid fibrils. A child with renal amyloidosis may present with proteinuria or nephrotic syndrome. Chronic renal failure may follow. Amyloid fibrils may deposit in other organs as well. The diagnosis is through the typical appearance on histopathology. Although chronic infections and chronic inflammatory diseases used to be the causes of secondary amyloidosis in children, the most frequent cause is now autoinflammatory diseases. "Renal amyloidosis in children." Bilginer Y, Akpolat T, Ozen S. Pediatr Nephrol. 2011 Mar 1. Autoinflammatory syndromes are characterised by recurrent or persistent inflammation with no increase in the antibody titers or antigen-specific T lymphocytes, and absence of infection. Initially, they included the hereditary periodic fever syndromes, a group of innate immune system monogenic diseases characterised by recurrent febrile episodes, with different characteristics, duration and interval, accompanied by other symptoms. Secondary amyloidosis is a complication in this group. The advances in the last few years has led to the identification of susceptible genes, new proteins, and characterising mechanisms and pathogenic routes that have led to an improvement in the diagnosis and establishing more effective treatments. Among these routes, are the changes in the inflammasome components, a group of cytoplasmic proteins that regulate the production of several inflammatory response mediators. The initial group of monogenic autoinflammatory diseases have increased in the last few years, due to including several polygenic hereditary diseases. "Autoinflammatory syndromes." Anton J. Med Clin (Barc). 2011 Jan;136 Suppl 1:3-9. Renal inflammation is a universal response to infectious and noninfectious triggers. Sensors of the innate immune system, such as Toll-like receptors or RIG-like receptors, provide danger recognition platforms on renal cells that integrate and translate the diverse triggers of renal inflammation by inducing cell activation and the secretion of proinflammatory cytokines and chemokines. As a new entry, the inflammasome-forming NLR genes integrate various danger signals into caspase-1-activating platforms that regulate the processing and secretion of pro-IL-1b and pro-IL-18 into the mature and active cytokines. Accumulating data now document a role for the NLRP3 inflammasome and IL-1b/IL-18 in many diseases, including atherosclerosis, diabetes, amyloidosis, malaria, crystal-related diseases, and other autoinflammatory disorders, identifying this innate immune pathway as an attractive therapeutic target. "The inflammasomes in kidney disease." Anders HJ, Muruve DA. J Am Soc Nephrol. 2011 Jun;22(6):1007-18. Epub 2011 May 12. Risk for amyloidosis in rheumatic diseases is associated with a long-lasting inflammation. "A marked decline in the incidence of renal replacement therapy for amyloidosis associated with inflammatory rheumatic diseases - data from nationwide registries in Finland." Immonen K, Finne P, Grnhagen-Riska C, Pettersson T, Klaukka T, Kautiainen H, Hakala M. Amyloid. 2011 Mar;18(1):25-8. Epub 2011 Feb 1. 
Amyotrophic lateral sclerosis (abbreviated ALS, also referred to as Lou Gehrig's disease) is a form of motor neuron disease caused by the degeneration of neurons located in the ventral horn of the spinal cord and the cortical neurons that provide their afferent input. Familial amyotrophic lateral sclerosis (FALS)-linked mutations in copper zinc superoxide dismutase (SOD1) cause motor neuron death through one or more acquired toxic properties. We analyzed the molecular mechanism underlying motor neuron degeneration in the transgenic mouse model expressing the SOD1 gene with G93A mutation. Our results suggest a mechanism of neurodegeneration that includes an inflammatory response as an important component. Thus, ALS has paralleled other neurodegenerative disorders, such as Alzheimer's and prion diseases, in which the inflammatory process is believed to participate directly in neuronal death. "Differential expression of inflammation- and apoptosis-related genes in spinal cords of a mutant SOD1 transgenic mouse model of familial amyotrophic lateral sclerosis." Tsuyoshi Yoshihara, Shinsuke Ishigaki, Masahiko Yamamoto, Yideng Liang, Jun, Ichi Niwa, Hideyuki Takeuchi, Manabu Doyu and Gen Sobue. Journal of Neurochemistry Volume 80, Issue 1, pages 158 167, January 2002 "Amyotrophic Lateral Sclerosis." Wikipedia en.wikipedia.org/wiki/Amyotrophic_lateral_sclerosis There is currently no effective pharmacological treatment for amyotrophic lateral sclerosis (ALS). Because recent evidence suggests that secondary inflammation and caspase activation may contribute to neurodegeneration in ALS, we tested the effects of minocycline, a second-generation tetracycline with anti-inflammatory properties, in mice expressing a mutant superoxide dismutase (SOD1G37R) linked to human ALS. Administration of minocycline into the diet, beginning at late presymptomatic stage (7 or 9 months of age), delayed the onset of motor neuron degeneration, muscle strength decline, and it increased the longevity of SOD1G37R mice by not, vert, similar5 weeks for not, vert, similar70% of tested mice. Moreover, less activation of microglia was detected at early symptomatic stage (46 weeks) and at the end stage of disease in the spinal cord of SOD1G37R mice treated with minocycline. These results indicate that minocycline, which is clinically well tolerated, may represent a novel and effective drug for treatment of ALS. "Minocycline Slows Disease Progression in a Mouse Model of Amyotrophic Lateral Sclerosis." Jasna Kriz, Minh Dang Nguyen and Jean-Pierre Julien. Neurobiology of Disease Volume 10, Issue 3, August 2002, Pages 268-278 
Anemia of inflammation develops in settings of chronic inflammatory, infectious, or neoplastic disease. In this highly prevalent form of anemia, inflammatory cytokines, including IL-6, stimulate hepatic expression of hepcidin, which negatively regulates iron bioavailability by inactivating ferroportin. "Inhibition of bone morphogenetic protein signaling attenuates anemia associated with inflammation." Steinbicker AU, Sachidanandan C, Vonner AJ, Yusuf RZ, Deng DY, Lai CS, Rauwerdink KM, Winn JC, Saez B, Cook CM, Szekely BA, Roy CN, Seehra JS, Cuny GD, Scadden DT, Peterson RT, Bloch KD, Yu PB. Blood. 2011 May 5;117(18):4915-23. Epub 2011 Mar 10. Cytopenias of uncertain etiology are commonly observed in patients during severe inflammation. Hemophagocytosis, the histological appearance of blood-eating macrophages, is seen in the disorder hemophagocytic lymphohistiocytosis and other inflammatory contexts. Although it is hypothesized that these phenomena are linked, the mechanisms facilitating acute inflammation-associated cytopenias are unknown. "Hemophagocytosis causes a consumptive anemia of inflammation." Zoller EE, Lykens JE, Terrell CE, Aliberti J, Filipovich AH, Henson PM, Jordan MB. J Exp Med. 2011 May 30. Between 30% and 90% of patients with cancer develop anemia due to direct effects of the disease, its treatment, underlying nutritional deficiencies, and the inflammation that characterizes chronic disease. "Iron replacement therapy in cancer-related anemia." Baribeault D, Auerbach M. Am J Health Syst Pharm. 2011 May 15;68(10 Suppl 1):S4-14; quiz S15-6. 
Adiponectin is a protein secreted by adipocytes which has anti-inflammatory properties. The objective of this study was to examine the relationship between adiponectinemia and the hemodynamic progression of aortic stenosis (AS) as well as the degree of inflammation in the valve explanted at the time of aortic valve replacement (AVR). "Hypoadiponectinemia Is Associated with Valvular Inflammation and Faster Disease Progression in Patients with Aortic Stenosis." Mohty D, Pibarot P, Cote N, Cartier A, Audet A, Despres JP, Mathieu P. Cardiology. 2011 May 19;118(2):140-146. This review presents optical molecular imaging as a promising tool that simultaneously detects pathobiological processes associated with inflammation and early stages of calcification in vivo at the (sub)cellular levels. Research into treatment of cardiovascular calcification is lacking, as shown by clinical trials that have failed to demonstrate the reduction of calcific aortic stenosis. Hence, the need to elucidate the pathways that contribute to cardiovascular calcification and to develop new therapeutic strategies to prevent or reverse calcification has driven investigations into the use of molecular imaging. This review discusses studies that have used molecular imaging methods to advance knowledge of cardiovascular calcification, focusing in particular on the inflammation-dependent mechanisms of arterial and aortic valve calcification. "Molecular imaging insights into early inflammatory stages of arterial and aortic valve calcification." New SE, Aikawa E. Circ Res. 2011 May 27;108(11):1381-91. In developed countries, calcific aortic stenosis (CAS) has become the most common acquired valvular disease. It is considered a for of atherosclerosis and, like the latter, of inflammatory origin. Our finding in the calcified cusps of both blood and lymphatic vessels together with lymphocytic infiltrates supports the inflammatory theory of the CAS pathogenesis. "Blood vessels and lymphatics in calcific aortic stenosis--in support of its inflammatory pathogenesis." Steiner I, Krbal L, Dominik J. Cesk Patol. 2010 Apr;46(2):33-6. 
The word "arthritis" means "inflammation of joints". It comes from two Greek words, athron meaning joints and its meaning inflammation. It is a chronic disease process. In the early stages, the whole body is usually involved and one or two joints may become completely deformed, leaving the patient handicapped and somewhat weakened. "Inflammation and Arthritis." DiseaseSatoz.com www.diseasesatoz.com/arthritis.htm Because arthritis is a disease of inflammation, the most effective and logical treatment is anything that fights inflammation. Medical management of arthritis usually starts with ibuprofen and other anti-inflammatory medications, and nutritional care starts with anti-inflammatory foods. "Fight arthritis with these foods." Joy Bauer, TODAY.com (2007) today.msnbc.msn.com/id/21246089/ns/today-today_health/t/fight-arthritis-these-foods Rheumatoid arthritis (RA) is a systemic, inflammatory disease. Renal involvement worsens the course of RA and increases mortality. It is suggested that chronic inflammatory processes may contribute to renal impairment. "Cystatin C concentration is correlated with disease activity in rheumatoid arthritis patients." Targoska-Stepniak B, Majdan M. Scand J Rheumatol. 2011 May 30. T helper 17 cells (Th17) have arisen in the last 15 years as major effector cells in several chronic inflammatory states. In synovitis associated with rheumatoid arthritis (RA), Th17 emerged as being involved in driving the active acute phases and correlated with local and systemic parameters of inflammation; in particular, TCRzeta(dim) Th17 appear to be the greatest producers of IL-17 at the single-cell level. "The potential role of Th17 in mediating the transition from acute to chronic autoimmune inflammation: rheumatoid arthritis as a model." Ferraccioli G, Zizzo G. Discov Med. 2011 May;11(60):413-24. Studying the influence on the immune system and role in inflammation of the sympathetic as well as the parasympathetic nervous system will not only increase our understanding of mechanism of disease, but could also lead to the identification of potential new therapeutic targets for chronic immune-mediated inflammatory diseases, such as rheumatoid arthritis (RA). "Restoring the balance of the autonomic nervous system as an innovative approach to the treatment of rheumatoid arthritis." Koopman FA, Stoof SP, Straub RH, Van Maanen MA, Vervoordeldonk MJ, Tak PP. Mol Med. 2011 May 20. doi: 10.2119/molmed.2011.00065. 
Severe asthma is characterized by elevated levels of pro-inflammatory cytokines and neutrophilic inflammation in the airways. Blood cytokines, markers of 'systemic' inflammation, may be a feature of amplified inflammation in severe asthma. "High serum levels of tumour necrosis factor-alpha and interleukin-8 in severe asthma: markers of systemic inflammation" M Silvestri, M Bontempelli, M Giacomelli, M Malerba, G A Rossi, A Di Stefano, A Rossi, F L M Ricciardolo. Clinical Immunology (2006) Volume: 36, Issue: 11, Pages: 1373-1381 Asthma is the most common chronic disease of childhood in industrialised countries. T helper-2 (Th-2) cells, mast cells and eosinophils have a role in inflammation of asthma. "Change of mean platelet volume values in asthmatic children as an inflammatory marker." Tuncel T, Uysal P, Hocaoglu AB, Erge DO, Karaman O, Uzuner N. Allergol Immunopathol (Madr). 2011 May 26. The clinical usefulness of fixed dose maintenance therapy using a combination inhaler containing budesonide and formoterol (FBC) has already been established, still evidence concerning anti-inflammatory effect by maintenance therapy with fix-dosed FBC, in comparison with other ICS and LABA combination therapy including salmeterol/fluticasone combination inhaler, is lacking. The number of patients who used SABA more than once a week has decreased 13 to 0 with FBC treatment. Conclusion: The airway anti-inflammatory effect by 8 weeks maintenance therapy with fix-dosed FBC 640/18 g/day (2 puffs twice a day) has been strongly suggested. "Clinical study concerning anti-inflammatory effect of fixed dose therapy by budesonide/formoterol combination inhaler for moderate persistent asthmatics." Hojo M, Mizutani T, Iikura M, Sugiyama A, Kobayashi N, Kudo K. Arerugi. 2011 May 30;60(5):575-585. 
Ataxia describes a lack of muscle coordination during voluntary movements, such as walking or picking up objects. A sign of an underlying condition, ataxia can affect your movements, your speech, your eye movements and your ability to swallow. Persistent ataxia usually results from damage to your cerebellum the part of your brain that controls muscle coordination. Many conditions may cause ataxia, including alcohol abuse, stroke, tumor, cerebral palsy and multiple sclerosis. It's also possible to inherit a defective gene that may cause one of many ataxia variants. Sharon McGrath-Morrow, MD, a pediatric pulmonologist with the A-T Clinical Center at Johns Hopkins Hospital, has found that levels of a pro-inflammatory molecule in the body called IL-8 are often elevated in patients with ataxia-telangiectasia (A-T). IL-8 is associated with premature cell aging, cancer progression and chronic inflammatory disorders. In her study, Dr. McGrath-Morrow found that IL-8 levels in patients with A-T were higher than that of patients with cystic fibrosis, non-A-T immunodeficiency, and healthy controls. These results, which have recently been accepted for publication in the Journal of Pediatrics, suggest that systemic inflammation may play a role in A-T. With further study, these findings may represent an avenue for potential therapy. Genetic disorders of iron metabolism and chronic inflammation often evoke local iron accumulation. In Friedreich ataxia, decreased iron-sulphur cluster and heme formation leads to mitochondrial iron accumulation and ensuing oxidative damage that primarily affects sensory neurons, the myocardium, and endocrine glands. "Ataxia." Mayo Clinic Staff, Mayo Clinic www.mayoclinic.com/health/ataxia/DS00910 "A-TCP and Wobbly Feet to Co-Fund Study about the Role of Inflammation in A-T." A-T Children's Project www.communityatcp.org/page.aspxpid=1696 "Selective iron chelation in Friedreich ataxia: biologic and clinical implications." Nathalie Boddaert, Kim Hanh Le Quan Sang, Agnes Rotig, Anne Leroy-Willig, Serge Gallet, Francis Brunelle, Daniel Sidi, Jean-Christophe Thalabard, Arnold Munnich, and Z. Ioav Cabantchik. Blood July 1, 2007 vol. 110 no. 1 401-408 Hypertrophic cardiomyopathy is a common complication of Friedreich's ataxia (FRDA). Histological sections reveal abnormal cardiomyocytes, muscle fiber necrosis, reactive inflammation, and increased endomysial connective tissue. "Iron and iron-responsive proteins in the cardiomyopathy of Friedreich's ataxia." Michael S, Petrocine SV, Qian J, Lamarche JB, Knutson MD, Garrick MD, Koeppen AH. Cerebellum. 2006;5(4):257-67. Machado-Joseph disease (MJD) also called spinocerebellar ataxia Type 3 (SCA3) is one of approximately 30 recognized, dominantly inherited forms of ataxia. Ataxia is a general term meaning lack of muscle control or coordination. MJD is characterized by slowly progressive clumsiness in the arms and legs, a staggering lurching gait that can be mistaken for drunkenness, difficulty with speech and swallowing, impaired eye movements sometimes accompanied by double vision or bulging eyes, and lower limb spasticity. Some individuals develop dystonia (sustained muscle contractions that cause twisting of the body and limbs, repetitive movements, and abnormal postures) or symptoms similar to those of Parkinson's disease. Others may develop fasciculations (twitching) of the face or tongue, neuropathy, or problems with urination and the autonomic nervous system. "Machado-Joseph Disease Fact Sheet." National Institute of Neurological Disorders and Stroke (March 18, 2011) www.ninds.nih.gov/disorders/machado_joseph/detail_machado_joseph.htm 
Epidemiological and experimental evidence has emerged that a dysregulated inflammation is associated with most of the tumors. Recent studies have begun to unravel molecular pathways linking inflammation and cancer. The identification of transcription factors such as NF-kappaB, STAT3, HIF-1 alpha and their gene products such as COX-2, cytokines, chemokines and chemokine receptors have laid molecular foundation for the decisive role of inflammation in carcinogenesis. Inflammation contributes to survival and proliferation of malignant cells, tumor angiogenesis, metastasis and reduced response to chemotherapy. In view of their involvement at different stages of tumor development, inflammatory pathways represent attractive targets for cancer prevention and therapy. "Targeting the inflammatory pathways to enhance chemotherapy of cancer." Zhu Z, Shen Z. Cancer Biol Ther. 2011 Aug 1;12(3). Extranodal non-Hodgkin lymphoma of the breast is a rare disease. We present a case of primary breast lymphoma with atypical clinical manifestations that looked like acute mastitis. A 46-year-old woman had noted a painful swelling in the right breast for 2 months. The mass had an inflammatory appearance and acute mastitis was the clinical impression. She underwent a core biopsy of the mass, and pathology showed inflammatory changes. The inflammatory mass regressed and recurred during hospitalization, and further incision with debridement was done. "Primary breast lymphoma clinically mimicking acute mastitis: a case report." Sun LM, Huang EY, Meng FY, Chang NJ, Chung LM, Liang JA, Lu CY. Tumori. 2011 Mar-Apr;97(2):233-5. doi: 10.1700/667.7790. Curcumin is a pleiotropic molecule against inflammatory related diseases. However, poor bioavailability greatly limits its application in clinic. Our previous study synthesized and evaluated a hydrosoluble mono-carbonyl analogue of curcumin, (2E,5E)-2,5-bis(4-(3-(dimethylamino)-propoxy)benzylidene)cyclopentanone (A13). In the present study, we further evaluated the anti-inflammatory effect of A13 in vivo. In lipopolysaccharide-challenged mice, pretreatment of A13 (15 mg/kg, i.v.) attenuated the increase of plasma level of NO, TNF-x, and IL-6, significantly inhibited the increase of hepatic inflammatory gene transcription, and improved pulmonary damages. In addition, A13 (10 or 30 mg/kg, i.p.) reduced vascular permeability in Institute of Cancer Research mice and inhibited pain reaction in chemically induced inflammatory models. Together, A13 exhibits anti-inflammatory activities both in vitro and in vivo by the inhibition of various inflammatory mediators. "A Novel Synthetic Mono-Carbonyl Analogue of Curcumin, A13, Exhibits Anti-Inflammatory Effects In vivo by Inhibition of Inflammatory Mediators." Wang Y, Yu C, Pan Y, Yang X, Huang Y, Feng Z, Li X, Yang S, Liang G. Inflammation. 2011 May 26. Findings from numerous studies suggest that inflammation is likely to have an important role in bladder carcinogenesis and cancer disease progression. While macrophages (Mos) constitute a major inflammatory component of the stroma of human bladder carcinoma, the regulatory role of such inflammatory leukocytes in tumor cell survival and invasion remains elusive. "Pro-inflammatory type-1 and anti-inflammatory type-2 macrophages differentially modulate cell survival and invasion of human bladder carcinoma T24 cells." Dufresne M, Dumas G, Asselin E, Carrier C, Pouliot M, Reyes-Moreno C. Mol Immunol. 2011 May 20. Inflammation plays a role in breast cancer progression and exercise has been reported to reduce inflammation; however, the anti-inflammatory effects of exercise in breast cancer have yet to be established. We examined the relationship between exercise training and systemic inflammation in relation to breast cancer progression in C3(1)SV40Tag mice. Female C3(1)SV40Tag mice were assigned to either exercise (Ex) or sedentary (Sed) treatment (n=12-14/group). Beginning at 4wks of age mice (Ex) were run on a treadmill for 60min/d (20m/min and 5% grade), 6d/wk for a period of 20wks. Mice were examined weekly for palpable tumors, and tumor number and volume were recorded. At 24wks of age mice were sacrificed and a more direct measure of tumor number and volume, and spleen weight was recorded. Plasma was analyzed for MCP-1 and IL-6 concentration using ELISA. Ex reduced palpable tumor number at sacrifice (24wks) by approximately 70% (P<0.05). Tumor volume was also reduced in Ex at 21-23wks (P<0.05). This reduction in tumor progression by Ex was associated with a reduction in plasma concentration of MCP-1 and IL-6, and spleen weight (P<0.05). These data provide strong support for a beneficial effect of exercise training on tumor progression in the C3(1)SV40Tag mouse model of breast cancer that may be partly mediated by its anti-inflammatory potential. "Benefits of exercise training on breast cancer progression and inflammation in C3(1)SV40Tag mice." Murphy EA, Davis JM, Barrilleaux TL, McClellan JL, Steiner JL, Carmichael MD, Pena MM, Hebert JR, Green JE. Cytokine. 2011 May 18. "Although there is plenty of evidence that chronic inflammation can promote cancer, the cause of this relationship is not understood," says Alexander Hoffmann, an assistant professor of chemistry and biochemistry at U.C. San Diego, who led the study. "We have identified a basic cellular mechanism that we think may be linking chronic inflammation and cancer." A protein called p100 allows communication between the inflammation and development processes. Some amount of dialogue is beneficial, but too much dialogue (which results from chronic inflammation) can lead to unrestrained development (cancer). "Studies with animals have shown that a little inflammation is necessary for the normal development of the immune system and other organ systems," explains Hoffmann. "We discovered that the protein p100 provides the cell with a way in which inflammation can influence development. But there can be too much of a good thing. In the case of chronic inflammation, the presence of too much p100 may over activate the developmental pathway, resulting in cancer." Chronic Inflammation & Chronic Disease, Allergy Consumer Report, Volume Four, Issue Two, February 2007 There is growing realization that cancer has a very strong inflammatory component. Therefore, it is likely that high-dose omega-3 fatty acids (EPA and DHA) could have a significant benefit for cancer patients. Published data indicates that cachexia can be reduced by high-dose fish oil. "Anti-Inflammatory Medicine: Dietary Modulation of Eicosanoids" Inflammation Research Foundation, Marblehead, MA www.inflammationresearchfoundation.org 
Celiac disease is an autoimmune disease characterized by an inappropriate immune response to dietary proteins found in wheat, rye, and barley (gluten and gliadin). This response leads to inflammation of the small intestine and to damage and destruction of the villi that line the intestinal wall. These villi are projections (small folds) that increase the surface area of the intestine and allow nutrients, vitamins, minerals, fluids, and electrolytes to be absorbed into the body. When the villi are destroyed, the body is much less capable of absorbing food and begins to develop symptoms associated with malnutrition and malabsorption. The damage and inflammation seen with celiac disease is associated with autoantibodies. When the body is exposed to the gluten and gliadin proteins, it forms antibodies that recognize and act against not only the grain proteins, but also against constituents of the intestinal villi. As long as the patient continues to be exposed to the proteins, he will continue to produce these autoantibodies. "Celiac Disease." American Association for Clinical Chemistry (Mar. 2011). www.labtestsonline.org/understanding/conditions/celiac.html Celiac disease is a permanent intolerance to the gliadin fraction of wheat gluten and to similar barley and rye proteins that occurs in genetically susceptible subjects. After ingestion, degraded gluten proteins reach the small intestine and trigger an inappropriate T cell-mediated immune response, which can result in intestinal mucosal inflammation and extraintestinal manifestations. "Enzymatic strategies to detoxify gluten: implications for celiac disease." Caputo I, Lepretti M, Martucciello S, Esposito C. Enzyme Res. 2010 Oct 7;2010:174354. Celiac disease (CD) is an autoimmune disorder of the small intestine that occurs in genetically predisposed people at all ages. However, it can be associated also to other immunopathological disorders, and may be associated with abnormal histology in segments of the gut other than the small bowel including colonic inflammation. "Celiac disease and microscopic colitis: A report of 4 cases." Barta Z, Zold E, Nagy A, Zeher M, Csipo I. World J Gastroenterol. 2011 Apr 28;17(16):2150-4. The cytosolic phospolypase A(2) (cPLA(2)) - dependent release of arachidonic acid (AA) from the intra-epithelial lymphocytes plays a pivotal role in arming lymphocytes to cytolysis in the immune response of celiac disease. However, little is known about the role of enterocytes in releasing AA. Docosahexaenoic acid (DHA) is a long chain polyunsaturated fatty acid that counteracts many of the proinflammatory effect of AA. The aims of the present work were to evaluate if: 1) intestinal epithelial cells have a role in the celiac inflammation, releasing AA, and 2) if DHA is able to modulate the celiac inflammation, down-regulating the release of AA. "Docosahexaenoic acid modulates in vitro the inflammation of celiac disease in intestinal epithelial cells via the inhibition of cPLA(2)." Vincentini O, Quaranta MG, Viora M, Agostoni C, Silano M. Clin Nutr. 2011 Mar 19. The gastrointestinal epithelium transports solutes and water between lumen and blood and at the same time forms a barrier between these compartments. This highly selective and regulated barrier permits ions, water, and nutrients to be absorbed, but normally restricts the passage of harmful molecules, bacteria, viruses and other pathogens. During inflammation, the intestinal barrier can be disrupted, indicated by a decrease in transcellular electrical resistance and an increase in paracellular permeability for tracers of different size. Such inflammatory processes are accompanied by increased oxidative stress, which in turn can impair the epithelial barrier. In this review, we discuss the role of inflammatory oxidative stress on barrier function with special attention on the epithelial tight junctions. Diseases discussed causing barrier changes include the inflammatory bowel diseases Crohn's disease, ulcerative colitis, and microscopic colitis, the autoimmune disorder celiac disease, and gastrointestinal infections. "Epithelial Barriers in Intestinal Inflammation." John LJ, Fromm M, Schulzke JD. Antioxid Redox Signal. 2011 May 11. 
Chronic fatigue syndrome (CFS) is a debilitating disease characterized by unexplained disabling fatigue and a combination of accompanying symptoms the pathology of which is incompletely understood. Many CFS patients complain of gut dysfunction. In fact, patients with CFS are more likely to report a previous diagnosis of irritable bowel syndrome (IBS), a common functional disorder of the gut, and experience IBS-related symptoms. The administration of probiotics could alter the gut microbiota, improve mucosal barrier function, decrease pro-inflammatory cytokines, and have the potential to positively influence mood in patients where both emotional symptoms and inflammatory immune signals are elevated. Probiotics also have the potential to improve gut motility, which is dysfunctional in many CFS patients. "Gut inflammation in chronic fatigue syndrome." Lakhan SE, Kirchgessner A. Nutr Metab (Lond). 2010 Oct 12;7:79. There is a significant 'comorbidity' between depression and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Depressive symptoms frequently occur during the course of ME/CFS. Fatigue and somatic symptoms (F&S), like pain, muscle tension, and a flu-like malaise, are key components of depression. At the same time, depression and ME/CFS show major clinical differences, which allow to discriminate them with a 100% accuracy. This paper aims to review the shared pathways that underpin both disorders and the pathways that discriminate them. Numerous studies have shown that depression and ME/CFS are characterized by shared aberrations in inflammatory, oxidative and nitrosative (IO&NS) pathways, like systemic inflammation and its long-term sequels, including O&NS-induced damage to fatty acids, proteins and DNA; dysfunctional mitochondria; lowered antioxidant levels, like zinc and coenzyme Q10; autoimmune responses to neoepitopes formed by O&NS; lowered omega-3 polyunsaturated fatty acid levels; and increased translocation of gram-negative bacteria. Some IO&NS-related pathways, like the induction of indoleamine 2-3-dioxygenase, neurodegeneration and decreased neurogenesis, are more specific to depression, whereas other pathways, like the 2'-5' oligoadenylate synthetase/RNase L pathway, are specific to ME/CFS. Most current animal models of depression, e.g. those induced by cytokines, are not reminiscent of human depression but reflect a mixture of depressive and F&S symptoms. The latter symptoms, sometimes called sickness behavior, differ from depression and ME/CFS because the former is a (sub)acute response to infection-induced pro-inflammatory cytokines that aims to enhance recovery, whereas the latter are characterized by long-term sequels in multiple IO&NS pathways. Depression and ME/CFS are not 'comorbid' disorders, but should be regarded as 'co-associated disorders' that are clinical manifestations of shared pathways. "An intriguing and hitherto unexplained co-occurrence: Depression and chronic fatigue syndrome are manifestations of shared inflammatory, oxidative and nitrosative (IO&NS) pathways." Maes M. Prog Neuropsychopharmacol Biol Psychiatry. 2011 Apr 29;35(3):784-94. Epub 2010 Jul 4. A new study conducted by researchers from Emory University and the Centers for Disease Control and Prevention (CDC) shows that individuals with chronic fatigue syndrome (CFS) have increased blood levels of the inflammatory chemicals known to increase risk for developing illnesses ranging from cardiovascular disease and dementia to diabetes and cancer. "Study Shows Inflammation from Chronic Fatigue Syndrome May be Risk Factor for Other Illnesses." Kathi Baker, The Robert W. Woodruff Health Sciences Center of Emory University insciences.org/article.phparticle_id=842 "Association of peripheral inflammatory markers with chronic fatigue in a population-based sample." Charles L. Raisona, Jin-Mann S. Lin and William C. Reeves. Brain, Behavior and Immunity, published on line Dec. 2008, DOI: 10.1016/j.bbi.2008.11.005 
COPD is caused by noxious particles or gas, most commonly from tobacco smoking, which triggers an abnormal inflammatory response in the lung. The inflammatory response in the larger airways is known as chronic bronchitis, which is diagnosed clinically when people regularly cough up sputum. In the alveoli, the inflammatory response causes destruction of the tissues of the lung, a process known as emphysema. "Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary." Rabe KF, Hurd S, Anzueto A, et al. (2007). Am. J. Respir. Crit. Care Med. 176 (6): 532 55. doi:10.1164/rccm.200703-456SO. PMID 17507545. "The Nature of Small-Airway Obstruction in Chronic Obstructive Pulmonary Disease." Hogg JC, Chu F, Utokaparch S, et al. (2004). N. Engl. J. Med. 350 (26): 2645 53. "Chronic obstructive pulmonary disease." Wikipedia en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_disease Chronic obstructive pulmonary disease (COPD) is the only chronic disease whose prevalence is increasing. It is the third cause of death wordwide, and it is projected to became the third in about ten years. COPD is strongly associated with cardiovascular diseases: this association is in part explained by risk factors in common (especially smoking), but in the latest years the hypothesis that COPD may cause a systemic inflammatory state, that in turn causes the increased risk of cardiovascular diseases in these patients, is taking over. "Chronic obstructive pulmonary disease and cardiovascular disease: role of the systemic inflammation." Rossi FF, Pedone C, Antonelli Incalzi R. Recenti Prog Med. 2011 Mar;102(3):109-113. doi: 10.1701/608.7066. Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation of the airways and progressive destruction of lung parenchyma. Apoptosis is critical for the maintenance of normal tissue homeostasis and is in equilibrium with proliferation and differentiation. This study was undertaken to investigate relationship between apoptosis of peripheral blood lymphocytes during exacerbation of COPD and inflammatory response that characterizes this condition. "Apoptosis of T lymphocytes isolated from peripheral blood of patients with acute exacerbation of chronic obstructive pulmonary disease." Lim SC, Ju JY, Chi SY, Ban HJ, Kwon YS, Oh IJ, Kim KS, Kim YI, Kim YC. Yonsei Med J. 2011 Jul 1;52(4):581-7. doi: 10.3349/ymj.2011.52.4.581. 
Sarcoidosis (from sarc meaning flesh, -oid, like, and -osis, process), also called sarcoid, Besnier-Boeck disease or Besnier-Boeck-Schaumann disease, is a disease in which abnormal collections of chronic inflammatory cells (granulomas) form as nodules in multiple organs. "Sarcoidosis." Talmadge E. King, Jr., MD, Merck Manual (2008) www.merckmanuals.com/home/sec04/ch050/ch050e.html Sarcoidosis is an inflammatory, granulomatous disease of unknown etiology that most commonly afflicts the lungs. In our study a strong systemic inflammatory profile was associated with sarcoidosis, with 29 analytes significantly elevated in sarcoidosis (false-discovery rate, <0.05 and >50% higher than controls). "Inflammatory profile and response to anti-tumor necrosis factor therapy in patients with chronic pulmonary sarcoidosis." Loza MJ, Brodmerkel C, Du Bois RM, Judson MA, Costabel U, Drent M, Kavuru M, Flavin S, Lo KH, Barnathan ES, Baughman RP. Clin Vaccine Immunol. 2011 Jun;18(6):931-9. Epub 2011 Apr 20. Sarcoidosis is a systemic granulomatous inflammation that occurs as a result of disturbed immune regulation in individuals exposed to certain environmental agents. Although tissue sampling is considered the "gold standard" for the diagnosis of sarcoidosis, a medically treated disease, minimally invasive diagnostic methods are preferred instead of surgical tissue sampling. "Diagnostic Value of Transbronchial Needle Aspiration Cytology in Sarcoidosis." Ozbudak IH, Ozblm G, Ozbudak O, Kovan TS. Turk Patoloji Derg. 2011;27(2):149-153. doi: 10.5146/tjpath.2011.01064. 
Chronic impaired venous outflow from the central nervous system has recently been claimed to be associated with multiple sclerosis (MS) pathology. This resulted in the term chronic cerebrospinal venous insufficiency (CCSVI) in MS. The concept of CCSVI is based on sonography studies showing that impaired venous outflow leading to pathological reflux is almost exclusively present in MS patients but not in healthy controls. Based on these findings, a new pathophysiological concept has been introduced suggesting that chronic venous outflow obstruction and venous reflux in the CNS result in pathological iron depositions leading to inflammation and neurodegeneration. "Chronic Cerebrospinal Venous Insufficiency" in Multiple Sclerosis - Is Multiple Sclerosis a Disease of the Cerebrospinal Venous Outflow System" Wattjes MP, Doepp F, Bendszus M, Fiehler J. Rofo. 2011 Jun;183(6):523-530. Epub 2011 Apr 12. The pathophysiology of venous dermal pathology in chronic venous disease (CVD) is reflective of a complex interplay that involves sustained venous hypertension, inflammation, cytokine and matrix metalloproteinase (MMP) activation, and altered cellular function. Ultimately, the persistent inflammatory-proteinase activity leads to advanced chronic venous insufficiency (CVI) and ulcer formation. "Dermal pathology, cellular biology, and inflammation in chronic venous disease." Raffetto JD. Thromb Res. 2009;123 Suppl 4:S66-71. CVD covers a full spectrum of venous conditions ranging from telangiectasias to the ultimate complications (venous ulcers). Symptoms are commonly associated with signs of CVD. What initiates the inflammatory events in venous valves and walls is not yet clear. It is likely that venous hypertension and subsequent stasis lead to vein distension which in turn allows venous flow reversal and areas of low shear stress. Even in the absence of reflux, endothelial cells which are exposed to flow reversal become activated, together with leukocytes which are activated by low shear stress. The leukocyte-endothelial interaction initiates and maintains inflammation. "Recent Guidelines in Chronic Venous Disease: the place of Daflon 500 mg." Francoise Pitsch, Phlebolymphology No. 69 Jan 2011. "Chronic venous disease." Bergan JJ, Schmid-Schnbein G, Coleridge-Smith P, Nicolaides A, Boisseau M, Eklof B. N Engl J Med. 2006;355:488- 498. 
Colitis is a term used to describe inflammation of the colon. There are a variety of causes of colitis including infections, poor blood supply, and autoimmune reactions. "Colitis." eMedicineHealth www.emedicinehealth.com/colitis/article_em.htm Ulcerative colitis (colitis ulcerosa) is a non-specific inflammatory bowel disease of unknown etiology. The symptoms which are observed in the course of ulcerative colitis are: an increase in the number of leukocytes and blood platelets, an increase in the concentration of IL-6 and anemia. Blood platelets are the key element, linking the processes of hemostasis, inflammation and the repair of damaged tissues. "Assessment of the influence of the inflammatory process on the activation of blood platelets and morphological parameters in patients with ulcerative colitis (colitis ulcerosa)." Polinska B, Matowicka-Karna J, Kemona H.Folia Histochem Cytobiol. 2011;49(1):119-24. The present study demonstrates the refractoriness of IEX-1 knockout (KO) mice to DSS-induced colitis and diminished pathogenesis of IEX-1-deficient CD4(+) CD45RB(hi) T cells. These data demonstrate that IEX-1 reciprocally regulates T-cell survival and apoptosis in a subset-dependent fashion. Inhibition of IEX-1 may thus offer novel strategies for colitis treatment by simultaneous induction of apoptosis in proinflammatory Th1 cells while promoting the survival and differentiation of a protective T-cell subset. (Inflamm Bowel Dis 2011;). "Reciprocal regulation of the survival and apoptosis of Th17 and Th1 cells in the colon." Ustyugova IV, Zhi L, Wu MX. Inflamm Bowel Dis. 2011 May 25. doi: 10.1002/ibd.21772. 
Crohn's disease is an ongoing disorder that causes inflammation of the digestive tract, also referred to as the gastrointestinal (GI) tract. Crohn's disease can affect any area of the GI tract, from the mouth to the anus, but it most commonly affects the lower part of the small intestine, called the ileum. The swelling extends deep into the lining of the affected organ. The swelling can cause pain and can make the intestines empty frequently, resulting in diarrhea. "Crohn's Disease." National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health. NIH Publication No. 06 3410 (2006). digestive.niddk.nih.gov/ddiseases/pubs/crohns Abstract Mastic (Pistacia lentiscus) of the Anacardiaceae family has exhibited anti-inflammatory and antioxidant properties in patients with Crohn's disease. This study was based on the hypothesis that mastic inhibits intestinal damage in inflammatory bowel disease, regulating inflammation and oxidative stress in intestinal epithelium. P. lentiscus powder could possibly have a therapeutic role in Crohn's disease, regulating oxidant/antioxidant balance and modulating inflammation. "Pistacia lentiscus Resin Regulates Intestinal Damage and Inflammation in Trinitrobenzene Sulfonic Acid-Induced Colitis." Gioxari A, Kaliora AC, Papalois A, Agrogiannis G, Triantafillidis JK, Andrikopoulos NK. J Med Food. 2011 May 25. The cause of Crohn's disease has not been mechanistically proven. We tested the hypothesis that the disease is a form of immunodeficiency caused by impaired innate immunity. We investigated inflammatory responses in patients and controls by quantifying neutrophil recruitment and cytokine production after acute trauma, interleukin 8 secretion by cultured monocyte-derived macrophages after exposure to inflammatory mediators, and local inflammatory and vascular changes in response to subcutaneous injection of heat-killed Escherichia coli. In Crohn's disease, a constitutionally weak immune response predisposes to accumulation of intestinal contents that breach the mucosal barrier of the bowel wall, resulting in granuloma formation and chronic inflammation. Polymorphisms in CARD15 do not underlie this phenotype, but incapacitate the NOD2 pathway that can compensate for impairment of innate inflammation. Current treatment of secondary chronic inflammation might exaggerate the underlying lesion and promote chronic disease. "Defective acute inflammation in Crohn's disease: a clinical investigation." Marks DJ, Harbord MW, MacAllister R, Rahman FZ, Young J, Al-Lazikani B, Lees W, Novelli M, Bloom S, Segal AW. Lancet. 2006 Feb 25;367(9511):668-78. 
Cystic fibrosis is characterized by excessive pulmonary inflammation, which presents early in life and becomes self-sustaining, eventually leading to the destruction of the lung. Treating inflammation is one of the most pressing needs in CF therapy and has been shown to slow lung function deterioration. "Methods for evaluating inflammation in cystic fibrosis." Ziady AG, Davis PB. Methods Mol Biol. 2011;742:51-76. Chronic inflammation of the lung, as a consequence of persistent bacterial infections by several opportunistic pathogens represents the main cause of mortality and morbidity in cystic fibrosis (CF) patients. "Dysfunctional CFTR Alters the Bactericidal Activity of Human Macrophages against Pseudomonas aeruginosa." Porto PD, Cifani N, Guarnieri S, Di Domenico EG, Mariggi MA, Spadaro F, Guglietta S, Anile M, Venuta F, Quattrucci S, Ascenzioni F. PLoS One. 2011;6(5):e19970. Epub 2011 May 18. Cystic fibrosis (CF) lung disease is characterized by progressive airflow obstruction, due to mucus plugging and inflammation within the bronchial walls, and destruction of the lung parenchyma secondary to bronchiectasis. These alterations result in an increase of the work of breathing, leading to alveolar hypoventilation predominantly during sleep, exercise and acute respiratory exacerbations. "Why, when and how to propose noninvasive ventilation in cystic fibrosis" Fauroux B. Minerva Anestesiol. 2011 May 20. 
For many years, a deficiency of monoamines including serotonin has been the prevailing hypothesis on depression, yet research has failed to confirm consistent relations between brain serotonin and depression. High degrees of overlapping comorbidities and common drug efficacies suggest that depression is one of a family of related conditions sometimes referred to as the "affective spectrum disorders", and variably including migraine, irritable bowel syndrome, chronic fatigue syndrome, fibromyalgia and generalized anxiety disorder, among many others. Herein, we present data from many different experimental modalities that strongly suggest components of mitochondrial dysfunction and inflammation in the pathogenesis of depression and other affective spectrum disorders. "Beyond the serotonin hypothesis: Mitochondria, inflammation and neurodegeneration in major depression and affective spectrum disorders." Gardner A, Boles RG. Prog Neuropsychopharmacol Biol Psychiatry. 2011 Apr 29;35(3):730-43. Epub 2010 Aug 5. Inflammation has been linked to depression and suicide risk. One inflammatory process that has been minimally investigated in this regard is cytokine-stimulated production of kynurenine (KYN) from tryptophan (TRP). Recent data suggest that KYN increases in cerebrospinal fluid (CSF) are associated with depressive symptoms secondary to immune activation. KYN may alter dopaminergic and glutamatergic tone, thereby contributing to increased arousal, agitation and impulsivity - important risk factors in suicide. We hypothesized that patients with major depressive disorder (MDD) and a history of suicide attempt would have higher levels of KYN than depressed nonattempters, who in turn would have higher levels than healthy volunteers. "Plasma kynurenine levels are elevated in suicide attempters with major depressive disorder." Sublette ME, Galfalvy HC, Fuchs D, Lapidus M, Grunebaum M, Oquendo MA, John Mann J, Postolache TT. Brain Behav Immun. 2011 May 14. Increasing evidence indicates that neuroinflammation plays an important role in some cases of major depression and also that antidepressants possess anti-neuroinflammatory properties. Inhibition of neuroinflammation may represent a novel mechanism of action of antidepressant treatment. "Antidepressants and Neuroinflammation: Can Antidepressants Calm Glial Rage Down" Hashioka S. Mini Rev Med Chem. 2011 May 16. As essential polyunsaturated fatty acids (PUFAs) influence both inflammatory and depressive disorders, nutrition related treatment methods deserve great research interest. However, currently biological mechanisms underlying the depression modulating effects of the PUFA Omega-3 (w-3) and Omega-6 (w-6) derived eicosanoids (central nervous system messengers) are not fully established. Depression related naturally occurring cell death (apoptosis) is thought to be mediated by excitotoxicity and free radicals that appear in the brain immediately following any inflammatory or ischemic damage, and increases the likelihood of clinically defined depression. This review explores the hypothesis that the interaction between w-6 and w-3 derived eicosanoids plays a central role in control over apoptosis linked with inflammation and inflammation-driven depression, via regulation of apoptosis inducing factors including excitotoxicity and free radicals. "What you eat is what you are - A role for polyunsaturated fatty acids in neuroinflammation induced depression" Pascoe MC, Crewther SG, Carey LM, Crewther DP. Clin Nutr. 2011 May 27. The emerging concept for pain-depression pathogenesis is the dysfunction of biogenic amine-mediated pain-depression control and the possible involvement of nitrodative stress-induced neurogenic inflammation. "Curcumin ameliorates reserpine-induced pain-depression dyad: Behavioural, biochemical, neurochemical and molecular evidences." Arora V, Kuhad A, Tiwari V, Chopra K. Psychoneuroendocrinology. 2011 May 23. Our data suggest that depressive symptoms are associated with preclinical y carotid atherosclerosis only if they are linked to inflammation, and that this association is present only in women. Underlying mechanisms are unknown but probably relate to adiposity. "Moderating effect of indoleamine 2,3-dioxygenase (IDO) activation in the association between depressive symptoms and carotid atherosclerosis: Evidence from the Young Finns study." Elovainio M, Hurme M, Jokela M, Pulkki-Raback L, Kivimaki M, Hintsanen M, Hintsa T, Lehtimaki T, Viikari J, Raitakari OT, Keltikangas-Jarvinen L. J Affect Disord. 2011 May 18. There is now evidence that depression, as characterized by melancholic symptoms, anxiety, and fatigue and somatic (F&S) symptoms, is the clinical expression of peripheral cell-mediated activation, inflammation and induction of oxidative and nitrosative stress (IO&NS) pathways and of central microglial activation, decreased neurogenesis and increased apoptosis. This review gives an explanation for the multiple "co-morbidities" between depression and a large variety of a) brain disorders related to neurodegeneration, e.g. Alzheimer's, Parkinson's and Huntington's disease, multiple sclerosis and stroke; b) medical disorders, such as cardiovascular disorder, chronic fatigue syndrome, chronic obstructive pulmonary disease, rheumatoid arthritis, psoriasis, systemic lupus erythematosus, inflammatory bowel disease, irritable bowel syndrome, leaky gut, diabetes type 1 and 2, obesity and the metabolic syndrome, and HIV infection; and c) conditions, such as hemodialysis, interferon--based immunotherapy, the postnatal period and psychosocial stressors. The common denominator of all those disorders/conditions is the presence of microglial activation and/or activation of peripheral IO&NS pathways. "Depression's multiple comorbidities explained by (neuro)inflammatory and oxidative & nitrosative stress pathways." Maes M, Kubera M, Obuchowiczwa E, Goehler L, Brzeszcz J. Neuro Endocrinol Lett. 2011 Feb 21;32(1):7-24. 
Currently an estimated 16 million people are afflicted with type 2 diabetes. This devastating disease puts a patient at a 2 to 4 times greater risk of dying from heart disease and also increases the likelihood of kidney failure, blindness, impotence, amputation, and neuropathy. Obviously a key to treating type 2 diabetes is the reversal of insulin resistance. Numerous studies indicate that insulin resistance is strongly associated with increased inflammation (74-76). It has been shown that when following an anti-inflammatory diet, insulin resistance can be reversed in three days (77). Not surprisingly, the composition of the anti-inflammatory diet is virtually identical to newest dietary recommendations from the Joslin Diabetes Research Center at Harvard Medical School for treating type 2 diabetes. "Anti-Inflammatory Medicine: Dietary Modulation of Eicosanoids" Inflammation Research Foundation, Marblehead, MA www.inflammationresearchfoundation.org In a study published in the July 18, 2001 issue of the Journal of the American Medical Association, a group from the famous Women's Health Study was evaluated to ascertain what risk factors could predict future development of Type II diabetes (Pradhan et al. 2001). The findings showed that baseline levels of C-reactive protein and interleukin-6 (IL-6) were significantly higher among those who subsequently developed diabetes compared to those who did not. When comparing the highest versus lowest quartile, women with the higher IL-6 levels were 7.5 times more likely to develop diabetes while those in the higher C-reactive protein ranges were 15.7 times more likely to become diabetic. After adjusting for all other known risk factors, women with the highest IL-6 levels were 2.3 times at greater risk, while those with the highest C-reactive protein levels were 4.2 times more likely to become diabetic. It should be noted that these other diabetic risk factors (such as obesity, estrogen replacement therapy and smoking) all sharply increase inflammatory markers in the blood. The doctors who conducted this study concluded by stating: "Elevated C-reactive protein and IL-6 predict the development of Type II diabetes mellitus. These data support a possible role for inflammation in diabetogenesis." Aging and Inflammation, LifeExtention.com www.lef.org/protocols/prtcl-146.shtml Obesity and type 2 diabetes are inflammatory conditions that should be successfully treated by anti-inflammatory interventions. One such intervention is the long-term use of a proposed anti-inflammatory diet that delivers the benefits of calorie-restriction and hormonal modulation that currently can only be achieved with gastric bypass surgery. This is especially true if that anti-inflammatory diet makes extensive use of products produced by molecular baking. "Anti-Inflammatory Medicine: Dietary Modulation of Eicosanoids" Inflammation Research Foundation, Marblehead, MA www.inflammationresearchfoundation.org Renal inflammation is a universal response to infectious and noninfectious triggers. Sensors of the innate immune system, such as Toll-like receptors or RIG-like receptors, provide danger recognition platforms on renal cells that integrate and translate the diverse triggers of renal inflammation by inducing cell activation and the secretion of proinflammatory cytokines and chemokines. As a new entry, the inflammasome-forming NLR genes integrate various danger signals into caspase-1-activating platforms that regulate the processing and secretion of pro-IL-1b and pro-IL-18 into the mature and active cytokines. Accumulating data now document a role for the NLRP3 inflammasome and IL-1b/IL-18 in many diseases, including atherosclerosis, diabetes, amyloidosis, malaria, crystal-related diseases, and other autoinflammatory disorders, identifying this innate immune pathway as an attractive therapeutic target. "The inflammasomes in kidney disease." Anders HJ, Muruve DA. J Am Soc Nephrol. 2011 Jun;22(6):1007-18. Epub 2011 May 12. We studied one hundred twenty-four consecutive outpatients with diabetes and 87 consecutive controls with a previous diagnosis of other endocrine disease. RLS was diagnosed in 22 diabetic patients (17.7%) and in only 5 controls (5.5%). This is the first controlled study confirming a significant association between RLS and type 2 diabetes. In diabetic patients, polyneuropathy represents the main risk factor for RLS. "Association of restless legs syndrome in type 2 diabetes: a case-control study." Merlino G, Fratticci L, Valente M, Del Giudice A, Noacco C, Dolso P, Cancelli I, Scalise A, Gigli GL. Sleep. 2007 Jul;30(7):866-71. 
Erectile dysfunction (ED) is highly prevalent among type 2 diabetes mellitus patients (T2DM). Although a link among systemic inflammation, endothelial dysfunction, and ED is described in clinical situations mainly related with coronary heart disease (CHD) risk, evidences of this link in T2DM patients are rather limited. Our aim was to evaluate the association between endothelial dysfunction and balance of pro-/anti-inflammatory mediators with ED presence and severity in T2DM. Our study showed that ED in T2DM patients without symptomatic CHD is associated with systemic endothelial dysfunction and a predominant, imbalanced low-grade inflammatory response. "Imbalanced Low-Grade Inflammation and Endothelial Activation in Patients with Type 2 Diabetes Mellitus and Erectile Dysfunction." Arana Rosainz MD, Ojeda MO, Acosta JR, Elas-Calles LC, Gonzalez NO, Herrera OT, Garcia Alvarez CT, Rodriguez EM, Baez ME, Seijas EA, Valdes RF. J Sex Med. 2011 May 6. doi: 10.1111/j.1743-6109.2011.02277.x. Periodontitis is a set of inflammatory diseases affecting the periodontium, i.e., the tissues that surround and support the teeth. Both chronic periodontal disease (CPD) and erectile dysfunction (ED) are associated with cardiovascular disease and its risk factors, including smoking and diabetes mellitus. However, the association between ED and CPD has never been studied. CPD was significantly more prevalent among men with mild ED (P = 0.004) and moderate to severe ED (P = 0.007) in comparison to men without ED. ED might be associated with CPD. These preliminary findings are consistent with theories that associate these conditions with systemic inflammation, endothelial dysfunction, and atherosclerosis. "Erectile dysfunction might be associated with chronic periodontal disease: two ends of the cardiovascular spectrum." Zadik Y, Bechor R, Galor S, Justo D, Heruti RJ. J Sex Med. 2009 Apr;6(4):1111-6. Epub 2008 Dec 15. "Periodontitis." Wikipedia en.wikipedia.org/wiki/Periodontitis The increased prevalence of erectile dysfunction (ED) has been reported in patients with chronic obstructive pulmonary disease, and sustained systemic inflammation seems to play a central role in this linkage. "Asthma and Risk of Erectile Dysfunction-A Nationwide Population-Based Study." Chou KT, Huang CC, Chen YM, Perng DW, Chao HS, Chan WL, Leu HB. J Sex Med. 2011 Jun;8(6):1754-1760. doi: 10.1111/j.1743-6109.2011.02242.x. Epub 2011 Mar 22. 
In times past, symptoms of inflammation were easy to identify; swelling, heat and pain. With newer emerging disorders such as fibromyalgia, lupus, chronic fatigue and multiple allergic response syndromes (MARS), to mention a few, identification and diagnosis is challenging. More often than not, inflammation in the soft and connective tissue is invisible to everyone except the victim. In the case of digestive disorders, many victims of leaky gut, Crohn's, colitis and irritable bowel never connect that part of the culprit can be the destruction of their oral health, subsequent bacterial inflammation and inflammation-causing foods. "Connecting Fibromyalgia, Inflammation and Oral Health." Invisible Illnesses, Gloria Gilbre, N.D., D.A.Hom., PhD., Freedom Publishing Company (IL) (February 2005) Formalin-fixed, paraffin-embedded skin tissue sections were collected from a matched cohort of 63 fibromyalgia syndrome (FMS) patients and 49 volunteers from the general population with both alpha1-antitrypsin (AAT) normal and deficiency variants. These tissues were examined for the expression of the broad-spectrum inhibitor AAT, the serine proteinases elastase and tryptase, the proinflammatory cytokines MCP-1 and TNFx, the endothelium biomarker VEGF, and the inflammation/nociception-related receptor PAR(2). The most relevant finding of the study was a significantly increased number of mast cells (MCs) in the papillary dermis of all FMS patients (greater than or equal to five to 14 per microscopic high power field) compared to zero to one in controls (p < 0.001). Our results indicate that FMS is a MC-associated condition. MCs are present in skin and mucosal surfaces throughout the human body, and are easily stimulated by a number of physical, psychological, and chemical triggers to degranulate, releasing several proinflammatory products which are able to generate nervous peripheral stimuli causing CNS hypersensitivity, local, and systemic symptoms. "Abnormal overexpression of mastocytes in skin biopsies of fibromyalgia patients." Blanco I, Beritze N, Arguelles M, Carcaba V, Fernandez F, Janciauskiene S, Oikonomopoulou K, de Serres FJ, Fernandez-Bustillo E, Hollenberg MD. Clin Rheumatol. 2010 Dec;29(12):1403-12. Epub 2010 Apr 30. Inflammation is an important mediator of increased sympathetic nervous system activity and may lead to pain in fibromyalgia patients. "Helicobacter pylori seropositivity in fibromyalgia syndrome." Akkaya N, Akkaya S, Polat Y, Turk M, Turk T, Turhal E, Sahin F. Clin Rheumatol. 2011 Jan;30(1):43-9. Epub 2010 Dec 1. Many researchers feel that chronic inflammation along with an altered immune system may either be the cause or contribute to fibromyalgia (FM) and chronic fatigue syndrome (CFS) symptoms. Fortunately, some treatment options are emerging to manage such inflammation and thus limit the discomfort and pain brought on by these ailments. Strong preliminary evidence leads many researchers to believe that excess cytokines may be responsible for CFS and FM symptoms. A degree of relief may be possible through present therapies, supplements and diet regimes. As more research reveals in greater detail the exact nature of immune dysfunction in these ailments, medications will likely be developed to more effectively alleviate cytokine inflammation in CFS and FM. Chemical messengers called cytokines form an integral part element of the immune system. As messengers, cytokines tell other immune cells to activate, grow or even die. Dr. Lionel Ivashkiv, a rheumatologist, explains that "cytokines regulate the immune system responses and can drive the inflammatory process." In this and other ways, cytokines aid white blood cells in fighting infection. "Cytokines Play an Aetiopathogenetic Role in Fibromyalgia: a Hypothesis and Pilot Study." Wallace, et al., Rheumatology, 40:743 (2001) "Neuroendocrine and Immune Aspects of Fibromyalgia, BioDrugs." West & Maes, 15(8):521 (2001) "A Natural Fibromyalgia Treatment Protocol." Dr. Zoltan P. Rona, M.D., MSc. (2002) ProHealth.com www.immunesupport.com/library/showarticle.cfmID=3364 The leaky gut syndrome is basically caused by inflammation of the gut lining. Inflammation causes the spaces between the cells to enlarge, allowing the absorption of large protein molecules which are usually broken down to much smaller pieces before absorption through the normally small spaces between the gut lining cells. The immune system starts making antibodies against the larger molecules because it recognizes it as a foreign, invading substance. Antibodies are made against the proteins and the previously well tolerated foods. These antibodies can get into various tissues and trigger an inflammatory reaction when the corresponding food is consumed. This occurs because body tissues have antigenic sites very similar to those on the foods, bacteria, parasites, candida or fungi. Autoantibodies are thus created and inflammation can become chronic. If this inflammation occurs in a joint, autoimmune arthritis develops. If it occurs in the blood vessels, vasculitis (inflammation of the blood vessels) is the resulting autoimmune problem. If it occurs in the muscles and multiple organ systems, the result may very well be FMS or ME/CFS. "A Natural Fibromyalgia Treatment Protocol." Dr. Zoltan P. Rona, M.D., MSc. (2002) ProHealth.com www.immunesupport.com/library/showarticle.cfmID=3364 "Chronic fatigue syndrome and myofascial pain syndrome." Goldenberg, Don. Fibromyalgia, Current Opinion in Rheumatology. 5:199-208 1993. "Diagnosis, etiology and therapy of fibromyalgia." Duna, George and Wilke, William. Comprehensive Therapy 19(2)60-63;1993. "Fibromyalgia: An explanation for the aches and pains of the nineties." Rothschild, Bruce. Comprehensive Therapy 17(6):9-14 1991. "Presence of anticardiolipin antibodies in the fibromyalgia syndrome." Romano TJ, Homburger HA. The Pain Clinic, 4(3):147-153, Sept. 1991. "Influenza A Virus: A Possible Precipitating Factor in Fibromyalgia" Tyler, Allen N. Alt Med Rev 1997;2(2):82-86). "Toward an integrated understanding of fibromyalgia syndrome." Boissevain MD, McCain GA. I. Medical and pathophysiological aspects. Pain, 45:227-238, 1991. 
Inflammation plays a role in heart disease because the immune system attacks LDL "bad" cholesterol that has been embedded in arterial walls. Ongoing inflammation eventually damages the arteries, which can cause them to burst. In fact, inflammation is so closely associated with heart disease that many doctors now use use a test for inflammation called CRP (C-reactive protein) to assess a person's risk of heart attack. Research shows that CRP can predict the risk of heart attack and stroke as well or better than cholesterol levels. This marker indicates an increased risk for destabilized atherosclerotic plaque and abnormal arterial clotting. When arterial plaque becomes destabilized, it can burst open and block the flow of blood through a coronary artery, resulting in an acute heart attack. One of the New England Journal of Medicine studies showed that people with high levels of C-reactive protein were almost three times as likely to die from a heart attack (Ridker et al. 1997). Chronic Inflammation & Chronic Disease, Allergy Consumer Report, Volume Four, Issue Two, February 2007 Aging and Inflammation, LifeExtention.com www.lef.org/protocols/prtcl-146.shtml A powerful statement on the role of anti-inflammatory diet in preventing heart disease mortality comes from the Lyon Diet Heart Study. In this study, heart attack survivors were split into two groups with one group put on a diet that followed the American Heart Association recommendations and the second group put on a diet similar to the previously described anti-inflammatory diet (rich in fruits, vegetables, and fish, but containing very low amounts of omega-6 fatty acids). Although, both groups had the same cholesterol levels and same triglycerides at the end of four years, there was, a more than a 70 percent reduction in both fatal and non-fatal heart attacks in anti-inflammatory diet group compared to the control diet group. More important, the group following the anti-inflammatory diet experienced no sudden deaths (a primary cause of cardiovascular mortality) during the four years of the study. The only clinical difference between the two groups that could explain such dramatic cardiovascular benefits was the reduction in the AA/EPA ratio. "Effect of a Mediterranean type of diet on the rate of cardiovascular complications in patients with coronary artery disease." deLorgeril M, Salen P, and Delaye J. J Amer Coll Cardiology 28: 1103-1108 (1996) "Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study." deLongeril M, Salen P, Martin JL, Monjaud I, Delaye J, and Mamelle N. Circulation 99: 779-785 (1999) "Anti-Inflammatory Medicine: Dietary Modulation of Eicosanoids" Inflammation Research Foundation, Marblehead, MA www.inflammationresearchfoundation.org The recent JELIS study has confirmed the benefits in cardiovascular outcome by lowering the AA/EPA ratio. In this study, more than 18,000 Japanese patients were put on statin therapy for four and a half years. Half of these patients received 1.8 grams per day of EPA, and the other half a placebo consisting of olive oil. Those receiving the extra EPA had their AA/EPA ratio reduced by 50%. At the conclusion of the study, those patients supplemented with EPA had had a 20-percent reduction in total cardiovascular events compared to those who were on the placebo. Thus a 20-percent reduction in cardiovascular events correlated with a 50-percent decrease in the AA/EPA ratio, whereas those on the placebo had no reduction in their AA/EPA ratio during the course of the study. The reason that EPA could have such a profound impact comes from the fact that statins are the only drugs known to increase the production of AA. Thus statins can increase silent inflammation. This may be the reason why the combination of statins and high-dose fish oil rich in EPA may represent a preferred method of improving outcomes in cardiovascular patients as demonstrated by the JELIS study. "Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis." Yokoyama M, Origasa H, Matsuzaki M, Matsuzawa Y, Saito Y, Ishikawa Y, Oikawa S, Sasaki J, Hishida H, Itakura H, Kita T, Kitabatake A, Nakaya N, Sakata T, Shimada K, and Shirato K. Lancet 369:1090-1098 (2007) "Statin treatment alters serum n-3 and n-6 fatty acids in hypercholesterolemic patients." Harris JI, Hibbeln JR, Mackey RH, and Muldoon MF. Prostaglandins Leukot Essent Fatty Acids 71: 263-269 (2004) "Anti-Inflammatory Medicine: Dietary Modulation of Eicosanoids" Inflammation Research Foundation, Marblehead, MA www.inflammationresearchfoundation.org 
HIV-associated inflammation and immunosenescence have been implicated as causally related to the premature onset of other end-organ diseases. Novel therapeutic strategies aimed at preventing or reversing these immunologic defects may be necessary if HIV-infected patients are to achieve normal life span. Chronic inflammation is strongly associated with the development of morbidity and mortality in the elderly and in those with HIV disease. Chronic viral infections such as the herpes and hepatitis viruses are an important cause of this persistent inflammation in both settings. CMV causes lifelong antigenic stimulation and the eventual development of an expanded population of well-differentiated, apoptosis-resistant, senescent T cells with limited proliferative potential. The end result is an immune system with limited capacity to recognize novel antigens and hence prevent disease. Because copathogens are more common in people with HIV, and because they appear to have a deleterious immunologic and clinical impact in HIV disease (58, 95), it seems reasonable to postulate coinfections may contribute to the "accelerated aging" syndrome now being observed in HIV-infected individuals. Approved drugs that have an anti-inflammatory effect and are often used in older adults-including aspirin, omega-3 fatty acids, vitamin D, and the statins-are now being studied as adjuncts to antiretroviral therapy in younger HIV-infected individuals. "HIV Infection, Inflammation, Immunosenescence, and Aging." Steven G. Deeks Annu. Rev. Med. 2011. 62:141 55 10.1146/annurev-med-042909-093756 Effros RB, Pawelec G. 1997. Replicative senescence of T cells: does the Hayflick Limit lead to immune exhaustion Immunol. Today 18:450 54 Targonski PV, Jacobson RM, Poland GA. 2007. Immunosenescence: role and measurement in influenza vaccine response among the elderly. Vaccine 25:3066 69 Hsue PY, Hunt PW, Sinclair E, et al. 2006. Increased carotid intima-media thickness in HIV patients is associated with increased cytomegalovirus-specific T-cell responses. AIDS 20:2275 83 Kovacs A, Al-Harthi L, Christensen S, et al. 2008. CD8+ T cell activation in women coinfected with human immunodeficiency virus type 1 and hepatitis C virus. J. Infect. Dis. 197:1402 7 Naeger DM,Martin JN, Sinclair E, et al. 2010. Cytomegalovirus-specific T cells persist at very high levels during long-term antiretroviral treatment of HIV disease. PLoS One 5:e8886 Human immunodeficiency virus (HIV) is a lentivirus (a member of the retrovirus family) that causes acquired immunodeficiency syndrome (AIDS) a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. "How does HIV cause AIDS?" Weiss RA (May 1993). Science 260 (5112): 1273 9. doi:10.1126/science.8493571. PMID 8493571. "Emerging concepts in the immunopathogenesis of AIDS." Douek DC, Roederer M, Koup RA (2009). Annu. Rev. Med. 60: 471 84. doi:10.1146/annurev.med.60.041807.123549. PMC 2716400. PMID 18947296. Diminished adult neurogenesis is considered a potential mechanism in the pathogenesis of HIV-1-associated dementia (HAD). In HAD, HIV-1-infected and immune-activated brain mononuclear phagocytes (MP; perivascular macrophages and microglia) drive central nervous system (CNS) inflammation and may alter normal neurogenesis. Inflammatory cytokines (including IL-6, IL-1a and TNF-a) produced by LPS-activated and/or HIV-1-infected MDM may contribute to MCM-induced STAT3 activation and astrocytic differentiation. These observations were confirmed in severe combined immunodeficient (SCID) mice with HIV-1 encephalitis (HIVE). This study generates important data elucidating the role of brain inflammation in neurogenesis and may provide insight into new therapeutic strategies for HAD. "HIV-1-Infected and Immune-Activated Macrophages Induce Astrocytic Differentiation of Human Cortical Neural Progenitor Cells via the STAT3 Pathway." Peng H, Sun L, Jia B, Lan X, Zhu B, Wu Y, Zheng J. PLoS One. 2011;6(5):e19439. Epub 2011 May 27. CD163, a haptoglobin-hemoglobin (Hp-Hb) scavenger receptor, expressed by monocytes and macrophages, is important in resolution of inflammation. Age-related non-AIDS co-morbidities in HIV-infected individuals, particularly dementia and cardiovascular disease, result in part from effects of HIV-1 infection on monocyte and macrophage biology. CD163 co-expression on CD14+CD16++ monocytes has been proposed as a useful biomarker for HIV-1 disease progression and the presence of HIV associated dementia. Our data show that all monocyte subsets are potentially capable of differentiating into CD163-expressing anti-inflammatory macrophages given appropriate stimuli. Levels of CD163 expression on monocytes may be a potential biomarker reflecting efforts by the immune system to resolve immune activation and inflammation in HIV-infected individuals. "Differential Expression of CD163 on Monocyte Subsets in Healthy and HIV-1 Infected Individuals." Tippett E, Cheng WJ, Westhorpe C, Cameron PU, Brew BJ, Lewin SR, Jaworowski A, Crowe SM. PLoS One. 2011;6(5):e19968. Epub 2011 May 20. HIV causes inflammation that can be at least partially corrected by HAART. To determine the qualitative and quantitative nature of cytokine perturbation, we compared cytokine patterns in three HIV clinical groups including HAART responders (HAART), untreated HIV non-controllers (NC), and HIV-uninfected (NEG). Our study shows that untreated, progress HIV infection was associated with decreased serum levels of cytokines important in T cell homeostasis (IL-15) and T cell phenotype determination (IL-12), and increased levels of innate inflammatory mediators such as IP-10 and TNF-a. "The effect of HIV infection and HAART on inflammatory biomarkers in a population-based cohort of US women." Keating SM, Golub ET, Nowicki M, Young M, Anastos K, Crystal H, Cohen MH, Zhang J, Greenblatt RM, Desai S, Wu S, Landay AL, Gange SJ, Norris PJ; and the Women's Interagency HIV Study. AIDS. 2011 May 12. Abstract HIV-related immune reconstitution inflammatory syndrome (IRIS) is increasingly being recognized in regions with a high burden of opportunistic infections. "Cryptococcal lymphadenitis and immune reconstitution inflammatory syndrome: Current considerations." Kuttiatt V, Sreenivasa P, Garg I, Shet A. Scand J Infect Dis. 2011 May 2. Viral blips in HIV controllers are associated with a significant decline in CD4 T cells and may be associated with an increased risk of pathological events, possibly owing to chronic inflammation/immune activation. "CD4 Dynamics over a 15 Year-Period among HIV Controllers Enrolled in the ANRS French Observatory." Boufassa F, Saez-Cirion A, Lechenadec J, Zucman D, Avettand-Fenoel V, Venet A, Rouzioux C, Delfraissy JF, Lambotte O, Meyer L; for the ANRS EP36 HIV Controllers Study Group. PLoS One. 2011 Apr 21;6(4):e18726. 
Inflammation is a critical component of cancer development. The clinical and pathological features of Hodgkin disease (HD) reflect an abnormal immunity that results from cytokines secreted by Reed-Sternberg cells and the surrounding tumor. Numerous studies have reported the association between genetic polymorphisms in cytokine genes and the susceptibility to different hematologic cancers. "Hodgkin disease risk: role of genetic polymorphisms and gene-gene interactions in inflammation pathway genes." Monroy CM, Cortes AC, Lopez MS, D'Amelio AM Jr, Etzel CJ, Younes A, Strom SS, El-Zein RA. Mol Carcinog. 2011 Jan;50(1):36-46. The association between chronic inflammation and cancer has been known for well over a century. However, direct evidence detailing the role of inflammation in carcinogenesis has been slow in forthcoming. A number of recent studies suggest that the gaps in our understanding of the molecular pathways bridging the link between inflammation and cancer are slowly beginning to close and that this relationship is more deep-rooted than had been previously believed. "Epstein-Barr virus, cytokines, and inflammation: a cocktail for the pathogenesis of Hodgkin's lymphoma?" Khan G. Exp Hematol. 2006 Apr;34(4):399-406. The effect of Hodgkin disease cells on the surrounding environment is complex. In the light of recent findings on growth factors and oncogenes a hypothesis on Hodgkin disease is presented. The interrelation of three main features of Hodgkin disease: malignancy, inflammation and abnormal immunity may be explained by the local secretion of platelet-derived growth factor like substances and interleukin-1 like substances by malignant Hodgkin disease cells. "Hodgkin disease: Malignancy, inflammation and abnormal immunity." Esther Aghai, Leukemia Research Volume 10, Issue 11, 1986, Pages 1267-1270 doi:10.1016/0145-2126(86)90332-2 
"When we found increased levels of cytokines in the brains of Huntington's disease patients, we were very excited," Moeller said. "Inflammation in the brain has been increasingly recognized as an important component in other neurodegenerative diseases such as Alzheimer's or Parkinson's disease. These findings might open the door to novel therapeutic approaches for Huntington's disease that target inflammation." "The protein could be causing damage through an abnormally overactive immune system in both the blood and the brain. While damage from Huntington's is typically seen in the brain, this new pathway is quite easy to detect in the blood of patients, so we may have found a unique window from the blood into what the disease is doing in the brain." The immune response in the blood may also help researchers use immune-system molecules as biological markers for the disease, which can be difficult to diagnose in early stages. Better tracking of Huntington's disease progression may help researchers to fine-tune interventions aimed at slowing the disease before it has affected as much brain tissue. "Huntington's Disease Linked To Overactive Immune Response In The Brain." University of Washington (2008, July 16). ScienceDaily. Retrieved June 10, 2011, from http://www.sciencedaily.com /releases/2008/07/080714141300.htm It is becoming increasingly clear that neuroinflammation is an integral component of Huntington's Disease. Httexp is expressed in microglial cells, the central effectors of neuroinflammation, and this expression alters several of the baseline parameters of these cells. However, the mechanism/s by which httexp causes the reported changes in microglial physiology is not well understood and thus is at the center of ongoing investigations in our and several other laboratories. Techniques similar to what has been employed to investigate neuronal transcriptional abnormalities (Cha 2007) will further our understanding on how httexp effects the microglial transcriptome. "Neuroinflammation in Huntington's disease," Thomas Moller, J Neural Transm DOI 10.1007/s00702-010-0430-7 (22 May 2010) Neuroinflammation is a prominent feature of many neurodegenerative diseases, however, little is known about neuroinflammation in Huntington's disease. We used quantitative real time-PCR to compare the expression level of neuroinflammation-associated mediators in the striatum, cortex, and cerebellum from post-mortem Huntington's disease patient samples with controls. We found increased expression of several key inflammatory mediators, including CCL2 and IL-10, specifically in the striatum of Huntington's disease patients, the main area affected by this pathology. Remarkably, we also found upregulation of IL-6, IL-8, and MMP9, in the cortex and notably the cerebellum, a brain area commonly thought to be spared by Huntington's disease. Our data suggest that neuroinflammation is a prominent feature associated with Huntington's disease and may constitute a novel target for therapeutic intervention. "Distinct neuroinflammatory profile in post-mortem human Huntington's disease." Silvestroni A, Faull RL, Strand AD, Moller T (2009) Neuroreport 20:1098 1103 
We set out to test the hypothesis that irritable bowel syndrome (IBS) is characterized by an augmented cellular immune response with enhanced production of proinflammatory cytokines. We further aimed to explore whether symptoms and psychiatric comorbidity in IBS are linked to the release of proinflammatory cytokines. Our study showed that patients with D-IBS display enhanced proinflammatory cytokine release, and this may be associated with symptoms and anxiety. "Immune Activation in Patients With Irritable Bowel Syndrome." Tobias Liebregts, Birgit Adam, Christoph Bredack, Alexander Roth, Susanne Heinzel, Sue Lester, Sarah Downie Doyle, Eric Smith, Paul Drew, Nicholas J. Talley and Gerald Holtmann. Presented in part at Digestive Disease Week 2006, Los Angeles, California, May 20-25, 2006. The pathogenesis of irritable bowel syndrome (IBS) is considered to be multifactorial and includes psychosocial factors, visceral hypersensitivity, infection, microbiota and immune activation. It is becoming increasingly clear that low-grade inflammation is present in IBS patients and a number of biomarkers have emerged. This review describes the evidence for low-grade inflammation in IBS and explores its mechanism with particular focus on gastrointestinal motor dysfunction. Understanding of the immunological basis of the altered gastrointestinal motor function in IBS may lead to new therapeutic strategies for IBS. "Low-grade inflammation plays a pivotal role in gastrointestinal dysfunction in irritable bowel syndrome." Akiho H, Ihara E, Nakamura K. World J Gastrointest Pathophysiol. 2010 Aug 15;1(3):97-105. The causes of irritable bowel syndrome (IBS) remain obscure. Some investigators have proposed chronic low-grade mucosal inflammation as a potential etiological factor. We performed a systematic review to examine this issue in detail. After testing, we conclude that low-grade mucosal inflammation, particularly mast cell activation, may be a contributory factor in the pathogenesis of IBS. Mast cell stabilizers warrant further assessment as a potential therapy in the condition. "Mucosal inflammation as a potential etiological factor in irritable bowel syndrome: a systematic review." Ford AC, Talley NJ. J Gastroenterol. 2011 Apr;46(4):421-31. Epub 2011 Feb 18. 
Inflammation is highly prevalent in patients with chronic kidney disease (CKD) and is consistently associated with cardiovascular morbidity and mortality. Clinical event rates increase with declining renal function and activation of the acute-phase response. "Statins, inflammation and kidney disease." Krane V, Wanner C; Medscape. Nat Rev Nephrol. 2011 May 31. In patients with end-stage renal disease (ESRD), inflammation, and protein energy wasting (PEW) are two highly prevalent and interconnected entities, jointly exerting a deleterious effect on multiple other ESRD-specific pathological processes and eventually on patient outcome. With respect to the pathophysiology underlying this strong association, knowledge has been actively expanded over the past few years. As such, it is nowadays recognized that inflammation acts via direct, as well as indirect, pathways in its contribution to PEW. Directly, inflammation causes alterations in amino acid utilization, translating into increased catabolism and decreased anabolism of muscle tissue. Indirectly, inflammation may act via altered ghrelin and adipokine metabolism, adipose tissue distribution, and pathological neuroendocrine signaling, as well as coexistent depression in inducing anorexia and PEW. In addition, two relatively new inflammatory markers (pentraxin-3 and TNF-like weak inducer of apoptosis) have gained attention with respect to their roles in this specific context. The current review deals with recent updates in the literature on the aforementioned pathways connecting inflammation to PEW and subsequent mortality. "Recent insights in inflammation-associated wasting in patients with chronic kidney disease." Meuwese CL, Carrero JJ, Stenvinkel P. Contrib Nephrol. 2011;171:120-6. Epub 2011 May 23. Chronic kidney disease is a worldwide growing problem in public health. It is a risk factor for complications in patients with acute coronary syndrome (ACS). Diabetes, hypertension (hypertrophy and left ventricular failure), impaired fibrinolysis and coagulation processes, as well as the rapid development of atherosclerosis (partly associated with chronic inflammation) are responsible for higher prevalence of cardiovascular diseases in patients with chronic kidney disease. "Chronic inflammation in patients with acute coronary syndrome and chronic kidney disease." Owczarek A, Babinska M, Szygula-Jurkiewicz B, Chudek J. Kardiol Pol. 2011;69(4):388-393. Low-fructose diet in subjects with CKD can reduce inflammation with some potential benefits on BP. Our pilot study needs to be confirmed by a larger clinical trial to determine the long-term benefit of a low-fructose diet compared to other diets in subjects with CKD. "Low-fructose diet lowers blood pressure and inflammation in patients with chronic kidney disease." Brymora A, Flisinski M, Johnson RJ, Goszka G, Stefanska A, Manitius J. Nephrol Dial Transplant. 2011 May 25. Renal inflammation is a universal response to infectious and noninfectious triggers. Sensors of the innate immune system, such as Toll-like receptors or RIG-like receptors, provide danger recognition platforms on renal cells that integrate and translate the diverse triggers of renal inflammation by inducing cell activation and the secretion of proinflammatory cytokines and chemokines. As a new entry, the inflammasome-forming NLR genes integrate various danger signals into caspase-1-activating platforms that regulate the processing and secretion of pro-IL-1b and pro-IL-18 into the mature and active cytokines. Accumulating data now document a role for the NLRP3 inflammasome and IL-1b/IL-18 in many diseases, including atherosclerosis, diabetes, amyloidosis, malaria, crystal-related diseases, and other autoinflammatory disorders, identifying this innate immune pathway as an attractive therapeutic target. "The inflammasomes in kidney disease." Anders HJ, Muruve DA. J Am Soc Nephrol. 2011 Jun;22(6):1007-18. Epub 2011 May 12. 
Liver disease (also called hepatic disease) is a broad term describing any single number of diseases affecting the liver. Hepatitis, inflammation of the liver, is caused mainly by various viruses but also by some poisons (e.g. alcohol), autoimmunity (autoimmune hepatitis) or hereditary conditions. "Liver Disease." Wikipedia en.wikipedia.org/wiki/Liver_disease Severe fatty liver is sometimes accompanied by inflammation, a situation that is referred to as steatohepatitis. Progression to alcoholic steatohepatitis (ASH) or non-alcoholic steatohepatitis (NASH) depend on persistence or severity of inciting cause. Pathological lesions in both conditions are similar. However, the extent of inflammatory response varies widely and does not always correlate with degree of fat accumulation. "Steatohepatitis: a tale of two "hits"?". Day CP, James OF (1998). Gastroenterology 114 (4): 842 5. doi:10.1016/S0016-5085(98)70599-2. PMID 9547102. Liver with extensive inflammation and high degree of steatosis often progresses to more severe forms of the disease. Hepatocyte ballooning and hepatocyte necrosis of varying degree are often present at this stage. Liver cell death and inflammatory responses lead to the activation of stellate cells which play a pivotal role in hepatic fibrosis. "Pathologic features associated with fibrosis in nonalcoholic fatty liver disease." Gramlich T, Kleiner DE, McCullough AJ, Matteoni CA, Boparai N, Younossi ZM (2004). Hum. Pathol. 35 (2): 196 9. doi:10.1016/j.humpath.2003.09.018. PMID 14991537. "Non-alcoholic fatty liver disease: an emerging pathological spectrum." Zafrani ES (2004). Virchows Arch. 444 (1): 3 12. doi:10.1007/s00428-003-0943-7. PMID 14685853. 
Inflammatory events persist in systemic lupus erythematosus (lupus) despite the use of anti-inflammatory (both steroidal and non-steroidal) and immunosuppressive drugs leading to delay in the healing/repair process and so tissue/organ damage continues. It is likely that lipoxins and other bioactive anti-inflammatory lipids such as resolvins, protectins, maresins and nitrolipids play a significant role in other auto-immune diseases such as rheumatoid arthritis, type 1 diabetes mellitus and multiple sclerosis and hence, could be of significant benefit in these diseases. "Lipoxins as biomarkers of lupus and other inflammatory conditions." Das UN. Lipids Health Dis. 2011 May 15;10(1):76. Systemic lupus erythematosus (SLE) with central nervous system (CNS) involvement is frequent and can have high morbidity. The primary pathophysiology of SLE in the CNS is thought to be inflammation secondary to autoantibody-mediated vasculitis. We interpret the SS-correlated increases in glucose consumption as potential evidence of inflammation, in keeping with prior reports of hypermetabolism in inflammatory disorders. To our knowledge, this is the first imaging evidence of SLE-induced CNS inflammation in an SLE inception cohort. "Neuroimaging evidence of white matter inflammation in newly diagnosed systemic lupus erythematosus." Ramage AE, Fox PT, Brey RL, Narayana S, Cykowski MD, Naqibuddin M, Sampedro M, Holliday SL, Franklin C, Wallace DJ, Weisman MH, Petri M. Arthritis Rheum. 2011 May 26. doi: 10.1002/art.30458. Imbalance oxidative stress and chemokines are considered as a universal factors involved in the development of various clinical features seen in the patients with SLE and arthritis. Our results indicate that excessive production of ROS disturbs redox status and can modulate the expression of inflammatory chemokines leading to inflammatory processes, exacerbating inflammation and affecting tissue damage in autoimmune diseases, as exemplified by their strong association with disease activity. "Interaction between oxidative stress and chemokines: Possible pathogenic role in systemic lupus erythematosus and rheumatoid arthritis." Shah D, Wanchu A, Bhatnagar A. Immunobiology. 2011 Apr 13. 
Abstract Lyme borreliosis is an arthropod-borne disease transmitted by the Ixodes tick. This spirochetal infection is first characterized by a local cutaneous inflammation, the erythema migrans. The skin constitutes a key interface in the development of the disease. During Borrelia inoculation, tick saliva affects the innate and adaptive immunity of the vertebrate host skin. Some key mediators of innate immunity such as antimicrobial peptides (cathelicidin and defensin families) have been identified as important initiators of skin inflammation. We analyzed the role of tick saliva on integumental innate immunity using different protocols of Borrelia infection, via syringe or direct tick transmission. "Tick Saliva Represses Innate Immunity and Cutaneous Inflammation in a Murine Model of Lyme Disease." Kern A, Collin E, Barthel C, Michel C, Jaulhac B, Boulanger N. Vector Borne Zoonotic Dis. 2011 May 25. The internalization of Borrelia burgdorferi, the causative agent of Lyme disease, by phagocytes is essential for an effective activation of the immune response to this pathogen. The intracellular, cytosolic receptor Nod2 has been shown to play varying roles in either enhancing or attenuating inflammation in response to different infectious agents. Nod2 suppresses Borrelia burgdorferi mediated murine Lyme arthritis and carditis through the induction of tolerance. Petnicki-Ocwieja T, DeFrancesco AS, Chung E, Darcy CT, Bronson RT, Kobayashi KS, Hu LT. PLoS One. 2011 Feb 28;6(2):e17414. Lyme disease (LD) is a seriously complex multi-system inflammatory disease that is triggered by the bacterial lipoproteins (BLPs) produced by the spiral-shaped bacteria called Borrelia. Borrelia are difficult to isolate, grow, and study in the laboratory. So, our technical knowledge of this pathogen is poor compared to our understanding of most bacteria that cause disease. Transmission of Borrelia occurs primarily through the bite of ticks. The disease affects every tissue and every major organ system in the body. Clinically, it can appear as a chronic arthalgia (joint pain), fibromyalgia (fibrous connective tissue and muscle pain), chronic fatigue, immune dysfunction and as neurological disease. LD may even be fatal in severe cases. "A Plague of Ignorance Regarding the Ignorance of a Plague." Dr Scott Taylor, DVM, Autoimmunity Research Foundation autoimmunityresearch.org/lyme-disease (2004) 
When the constriction of blood vessels in the brain stops and the aura subsides, the blood vessels of the scalp dilate. The walls of these blood vessels become permeable and some fluid leaks out. This leakage is recognized by pain receptors in the blood vessels of surrounding tissue. In response, the body supplies the area with chemicals which cause inflammation. With each heart beat, blood passes through this sensitive area causing a throb of pain. When certain nerves or an area in the brain stem become irritated, a migraine begins. In response to the irritation, the body releases chemicals which cause inflammation of the blood vessels. These chemicals cause further irritation of the nerves and blood vessels and results in pain. "Pathophysiology of the migraine aura. The spreading depression theory". Lauritzen M (February 1994). Brain 117 (1): 199 210. doi:10.1093/brain/117.1.199. PMID 7908596. "What Your Doctor May Not Tell You About(TM): Migraines : The Breakthrough Program That Can Help End Your Pain." Alexander Mauskop; Fox, Barry (2001). New York: Warner Books. ISBN 0-446-67826-0 "Migraine." Wikipedia en.wikipedia.org/wiki/Migraine Significant recent advances in molecular pharmacology have elucidated the molecular pathways involved in neurogenic inflammation (NI). The release of tachykinins and endothelin-3 (ET-3) from trigeminal neurons induces dural vascular permeability and vasodilatation via activation of tachykinin receptor 1 (Tacr1) and endothelin receptor type B (Ednrb) on endothelial cells. Endothelial cell receptor stimulation results in cellular contraction, leading to plasma protein extravasation (PPE), which is the most recognized physiological hallmark of NI, and nitric oxide-induced vasodilatation. "Neurogenic inflammation and migraine: implications for the therapeutics." Peroutka SJ. Mol Interv. 2005 Oct;5(5):304-11. The potential involvement of neurogenic inflammation in the pathogenesis of the migraine headache and the inhibition of this mechanism as a possible mode of action of antimigraine medications are discussed in great depth in this volume. The topics are approached from a pathophysiological as well as a clinical experimental perspective by a renowned group of clinicians and scientists who carefully consider the current, future, and potential therapeutic approaches to migraine treatment. "Migraine: A Neuroinflammatory Disease? (Progress in Inflammation Research)." Egilius L.H. Spierings (Editor), Margarita del Rio Sanchez (Editor) Birkhauser Basel; 1st edition (March 22, 2002) ISBN-13: 978-3764362317 What is the role of inflammation in migraine? The clinical data showing therapeutic efficacy of aspirin and NSAIDs are abundant and strong, as are the data for prednisone and other steroids, albeit when used in a defined context and for shorter time May 2005 NEUROLOGY 64(Suppl 2) S13 periods. We infer from these data and those summarized above that inflammation is an important component in a subset of migraineurs, perhaps genetically determined. "Migraine as an inflammatory disorder." Christian Waeber and Michael A. Moskowitz, Neurology May 24, 2005 64:S9-S15 
Multiple sclerosis (MS) is a disease of the central nervous system of unknown cause. There are many medications available for the disease, but none are clearly effective in ameliorating its long-term disabling effects. MS is felt to be most likely either due to an aberrant immune response or a pathogen, or possibly a combination of the two, and the animal models available reflect these two possible pathogeneses. The hallmarks of the disease are demyelination, inflammation, axonal injury, and progressive disability. "Experimental models of multiple sclerosis." Pachner AR. Curr Opin Neurol. 2011 Jun;24(3):291-9. The cause of MS remains unknown, but an autoimmune reaction against oligodendrocytes and myelin is generally assumed to play a major role, and early acute MS lesions almost invariably show prominent inflammation. "Adult stem cells and multiple sclerosis." Scolding N. Cell Prolif. 2011 Apr;44 Suppl 1:35-8. doi: 10.1111/j.1365-2184.2010.00721.x. Biopsy revealed an inflammatory subpial lesion containing lymphocytes and myelin-laden macrophages. Recurrent relapses with dissemination of MRI-typical white matter lesions characterized the subsequent course. Our findings highlight that cortical demyelination occurs on a background of inflammation and suggest that the noninflammatory character of chronic cortical demyelination may relate to long intervals between lesion formation and autopsy. This case provides pathologic evidence of relapsing-remitting MS presenting with inflammatory cortical demyelination and emphasizes the importance of considering demyelinating disease in the differential diagnosis of patients presenting with a solitary cortical enhancing lesion. "A case of multiple sclerosis presenting with inflammatory cortical demyelination." Popescu BF, Bunyan RF, Parisi JE, Ransohoff RM, Lucchinetti CF. Neurology. 2011 May 17;76(20):1705-10. Systemic autoinflammatory diseases are genetic disorders characterized by seemingly unprovoked inflammation, without major involvement of the adaptive immune system. Among them it is recognized the TNF receptor associated periodic syndrome (TRAPS) caused by mutations in the TNFRSF1A gene and characterized by symptoms such as recurrent high fevers, rash, abdominal pain, arthralgia and myalgia. Recent studies have recognized the potential role of TNFRSF1A mutations in Multiple Sclerosis (MS). "TNFSFR1A R92Q mutation, autoinflammatory symptoms and multiple sclerosis in a cohort from Argentina." Kauffman MA, Gonzalez-Morn D, Garcea O, Villa AM. Mol Biol Rep. 2011 May 13. Targeted migration is a necessary attribute for any gene delivery vehicle. Mesenchymal stem cells (MSC) have been used as effective delivery vehicles for treatments against cancer, graft versus host disease, -arthritis, multiple sclerosis, and many other diseases. MSC migrate toward sites of inflammation, however, the true migratory mechanism has yet to be elucidated. "Dissecting Mesenchymal Stem Cell Movement: Migration Assays for Tracing and Deducing Cell Migration." Spaeth EL, Marini FC. Methods Mol Biol. 2011;750:241-259. Inflammation on brain MRI is the most sensitive marker of disease activity in multiple sclerosis (MS) but its clinical consequences remain controversial. "Clinical consequences of MRI activity in treated multiple sclerosis." Cadavid D, Kim S, Peng B, Skurnick J, Younes M, Hill J, Wolansky LJ, Cook SD. Mult Scler. 2011 May 25. Th17 cells are a highly pro-inflammatory T-helper cell subset characterised by the expression of IL17. They have been implicated in a variety of allergic and autoimmune conditions. T-regulatory (Treg) cells, a subset of CD4 cells which express Foxp3, CD25, IL10 and TGFB, can suppress the activity of Th17 cells. In this study, we show that the circulating levels of Th17 and Treg cells in peripheral blood are correlated; furthermore, the expression of the pro-inflammatory cytokine IL17 and the anti-inflammatory cytokine IL10 by CD4 cells are also correlated. However, we found no clear correlation between cerebrospinal fluid (CSF) IL10 and IL17 cytokine levels in MS, approaching a negative correlation at the time of relapse, and an overall negative correlation between CSF IL17 and TGFB levels, suggesting a lack of central regulation of pro:anti-inflammatory balance in this demyelinating condition. "Central inflammation versus peripheral regulation in multiple sclerosis." Edwards LJ, Sharrack B, Ismail A, Tumani H, Constantinescu CS. J Neurol. 2011 Mar 9. Progranulin (PGRN) is a fundamental neurotrophic factor, and is also involved in inflammation and wound repair. PGRN may have pro- or anti-inflammatory properties, depending upon proteolysis of the anti-inflammatory parent PGRN protein and the generation of pro-inflammatory granulin peptides. PGRN is strongly expressed in MS brains, by macrophages/microglia in active lesions, and by activated microglia in the NAWM; PGRN CSF concentrations in MS are correspondingly increased in conditions of enhanced macrophage/microglia activation, such as during relapses and in progressive MS. "Progranulin expression in brain tissue and cerebrospinal fluid levels in multiple sclerosis." Vercellino M, Grifoni S, Romagnolo A, Masera S, Mattioda A, Trebini C, Chiavazza C, Caligiana L, Capello E, Mancardi GL, Giobbe D, Mutani R, Giordana MT, Cavalla P. Mult Scler. 2011 May 25. Cyclophosphamide (cy) is an alkylating agent used to treat malignancies and immune-mediated inflammatory nonmalignant processes. It has been used as a treatment in cases of worsening multiple sclerosis (MS). Cy is currently used for patients whose disease is not controlled by beta-interferon or glatiramer acetate as well as those with rapidly worsening MS. The most commonly used regimens involve outpatient IV pulse therapy given with or without corticosteroids every 4 to 8 weeks. Side effects include nausea, headache, alopecia, pain, male and women infertility, bladder toxicity, and risk of malignancy. Previous studies suggest that cy is effective in patients in the earlier stages of disease, where inflammation predominates over degenerative processes. Given that early inflammatory events appear to correlate with later disability, a major question is whether strong anti-inflammatory drugs, such as cy, will have an impact on later degenerative changes if given early in the disease to halt inflammation. "Lights and shadows of cyclophosphamide in the treatment of multiple sclerosis." Patti F, Lo Fermo S. Autoimmune Dis. 2011 Mar 15;2011:961702. Literature includes evidence of initial predominance of inflammation and later development of neurodegeneration in the pathogenesis of multiple sclerosis (MS). "Degenerative and inflammatory markers in the cerebrospinal fluid of multiple sclerosis patients with relapsing-remitting course of disease and after clinical isolated syndrome." Sladkova V, Mare J, Lubenova B, Zapletalova J, Stejskal D, Hlustik P, Kanovsky P. Neurol Res. 2011 May;33(4):415-20. Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS), characterized by inflammation, demyelination and axonal loss underlying progressive clinical disability. The chronic inflammatory tissue damage involving myelin and axons is driven by autoreactive T cells and represents a key mechanism in the immunopathogenesis of MS. Over the last few years, evidence from MS and experimental models of neuroinflammation has suggested that autoimmune responses could exert neuroprotective effects through the release of neurotrophins by autoreactive T cells. Specifically, the role of the Brain-derived neurotrophic factor (BDNF) in facilitating brain tissue repair in experimental traumatic injury has been well recognized. "Neuroinflammation and neuroprotection: an update on (future) neurotrophin-related strategies in multiple sclerosis treatment." De Santi L, Polimeni G, Cuzzocrea S, Esposito E, Sessa E, Annunziata P, Bramanti P. Curr Med Chem. 2011;18(12):1775-84. 
A moderate but selective increase in C-reactive protein in hypocretin-1 deficient subjects should prompt research on inflammation in narcolepsy. "CSF versus serum leptin in narcolepsy: is there an effect of hypocretin deficiency?" Arnulf I, Lin L, Zhang J, Russell IJ, Ripley B, Einen M, Nevsimalova S, Bassetti C, Bourgin P, Nishino S, Mignot E. Sleep. 2006 Aug;29(8):1017-24. The number of hypocretin-containing neurons is markedly decreased in most patients with the sleep disorder narcolepsy. It is presently not known why the loss of hypocretin neurons occurs in these patients. In the present study, we tested the role of inflammation in the degeneration of hypocretin neurons. The loss of hypocretin neurons produced by chronic LPS administration suggests that inflammation may play a role in the loss of hypocretin neurons in narcolepsy. "Effects of inflammation produced by chronic lipopolysaccharide administration on the survival of hypocretin neurons and sleep." Gerashchenko D, Shiromani PJ. Brain Res. 2004 Sep 3;1019(1-2):162-9. Siegel and other investigators have now found that the human brand of this puzzling sleep disorder likely stems from the destruction of a small group of brain cells. In the four narcoleptic brains his team studied, 5 to 15 percent of the hypocretin-containing cells remained in place. Furthermore, Siegel and his colleagues documented evidence of gliosis, a proliferation of brain cells called glia, at the site of cell loss. Gliosis, which is often the result of inflammation within the brain, hints at a possible cause of the brain-cell loss in narcolepsy, says Siegel. For more than 2 decades, scientists have suspected that the disorder is the result of the body's immune system attacking its own tissue. Determining what kills the hypocretin-making cells is crucial. Drugs that limit inflammation could fight narcolepsy if it indeed is an autoimmune disorder. "Brain-Cell Loss Found in Narcolepsy." J. Travis. CBS Interactive (2010). findarticles.com/p/articles/mi_m1200/is_10_158/ai_65913254 
Connective tissue disorders and chronic inflammation can cause direct and indirect nerve damage. When the multiple layers of protective tissue surrounding nerves become inflamed, the inflammation can spread directly into nerve fibers. Chronic inflammation also leads to the progressive destruction of connective tissue, making nerve fibers more vulnerable to compression injuries and infections. Joints can become inflamed and swollen and entrap nerves, causing pain. Some neuropathies are caused by inflammation resulting from immune system activities rather than from direct damage by infectious organisms. Inflammatory neuropathies can develop quickly or slowly, and chronic forms can exhibit a pattern of alternating remission and relapse. Peripheral neuropathy describes damage to the peripheral nervous system, the vast communications network that transmits information from the brain and spinal cord (the central nervous system) to every other part of the body. Peripheral nerves also send sensory information back to the brain and spinal cord, such as a message that the feet are cold or a finger is burned. Damage to the peripheral nervous system interferes with these vital connections. Like static on a telephone line, peripheral neuropathy distorts and sometimes interrupts messages between the brain and the rest of the body. More than 100 types of peripheral neuropathy have been identified, each with its own characteristic set of symptoms, pattern of development, and prognosis. Neuritis is a general term for inflammation of a nerve or the general inflammation of the peripheral nervous system. Symptoms depend on the nerves involved, but may include pain, paresthesia (pins & needles), paresis (weakness), hypoesthesia (numbness), anesthesia, paralysis, wasting, and disappearance of the reflexes. Acute inflammatory demyelinating neuropathy, better known as Guillain-Barre syndrome, can damage motor, sensory, and autonomic nerve fibers. Most people recover from this syndrome although severe cases can be life threatening. In a radiculopathy, the problem is at or near the root of the nerve, along the spine. However, the pain or other symptoms may manifest in an extremity through a process called referred pain. Chronic inflammatory demyelinating polyneuropathy (CIDP), usually damages sensory and motor nerves, leaving autonomic nerves intact. Multifocal motor neuropathy is a form of inflammatory neuropathy that affects motor nerves exclusively; it may be chronic or acute. Some forms of neuropathy involve damage to only one nerve and are called mononeuropathies. "Peripheral Neuropathy Fact Sheet." National Institute of Neurological Disorders and Stroke (February 18, 2011) www.ninds.nih.gov/disorders/peripheralneuropathy/detail_peripheralneuropathy.htm Vasculitis is a systemic illness with inflammation in the blood vessels. The inflammation may lead to occlusion of blood vessels and subsequent ischemia in the organs and tissues. When the inflammation is in the blood vessels supplying peripheral nerves, patients may develop vasculitic neuropathy. "Vasculitic Neuropathy." Johns Hopkins University www.hopkinsmedicine.org/neurology_neurosurgery/conditions_main/old/vasculitic_neuropathy.html A new Mayo Clinic study found that nerve inflammation may cause the pain, numbness and weakness following surgical procedures that is known as postsurgical neuropathy. "Inflammation Causes Some Postsurgical Neuropathies." Science Daily, Sep. 22, 2011 www.sciencedaily.com/releases/2010/09/100922111432.htm 
Obesity and type 2 diabetes are inflammatory conditions that should be successfully treated by anti-inflammatory interventions. One such intervention is the long-term use of a proposed anti-inflammatory diet that delivers the benefits of calorie-restriction and hormonal modulation that currently can only be achieved with gastric bypass surgery. This is especially true if that anti-inflammatory diet makes extensive use of products produced by molecular baking. It has been demonstrated at Harvard Medical School using iso-caloric diets that the ratio of protein to carbohydrate found in an anti-inflammatory diet gave superior reductions of elevated markers of inflammation when compared to an iso-caloric diet based on the USDA Food Pyramid (29). Likewise it has been shown that an anti-inflammatory diet generates reduction in silent inflammation, whereas an iso-caloric Atkins diet significantly increases silent inflammation. "Anti-Inflammatory Medicine: Dietary Modulation of Eicosanoids" Inflammation Research Foundation, Marblehead, MA www.inflammationresearchfoundation.org The body has a unique way of initially dealing with elevated AA levels that would otherwise increase silent inflammation. This is through the generation of healthy new fat cells. Derivatives of AA can stimulate the stem cells in the adipose tissue to create new fat cells for the purpose of storing any excess AA, and thus preventing it from circulating in the blood. In fact, the definition of a healthy fat cell is one that can increase the storage of triglycerides. By doing this, the adipose tissue if composed of healthy fat cells, becomes analogous to a toxic waste dump that sequesters any increased production of AA. This is clearly illustrated in children in which the greater the BMI, the higher the levels of AA in the adipose tissue. "Arachidonic acid and prostacylin signaling promote adipose tissue development: a human health concern" Massiera F, Saint-Marc P, Sedoux J, Murata T, Kobayshi T, Marumiya S, Guesnet P, Amri, E-Z, Megrel R, Ailhaud G: J Lipid Res 44:271-279, 2003 "Endogenous 15-deoxy-delta(12,14)-prostaglandin J(2) synthesized by adipocytes during maturation phase contributes to upregulation of fat storage." Mazid MA, Chowdhury AA, Nagao K, Nishimura K, Jisaka M, Nagaya T, Yokota K: FEBS Lett 580:6885-6890, 2006 "Association of adipose tissue arachidonic acid content with BMI and overweight status in children from Cyprus and Crete." Savva SC, Chadjigeorgiou C, Hatzis C, Kyriakakis M, Tsimbinos G, Tornaritis M, Kafatos A: Br J Nutr 91: 643-649, 2004 "Anti-Inflammatory Medicine: Dietary Modulation of Eicosanoids" Inflammation Research Foundation, Marblehead, MA www.inflammationresearchfoundation.org The problem begins when AA levels become too great in a particular fat cell. The fat cell response to insulin signaling becomes compromised due to internal inflammation. This interrupts the flow of glucose into the fat cell to provide the necessary glycerol for fatty acid storage. As a result, the fat cell has a more difficult time sequestering newly formed AA as well as other fatty acids. At the same time, insulin inhibition of the hormone sensitive lipase becomes compromised because of the same disruption in insulin signaling. These are the hallmarks of insulin resistance in the fat cell that arise far earlier than insulin resistance in muscle cells. As a result, not only do greater amounts of AA remain in circulation to be taken up by other cells potentially leading to insulin resistance in the muscle cells (causing increased hyperinsulinemia), but also the compromised fat cell is releasing greater amounts of previously sequestered AA from fat cells into the circulation. "Adipose tissue arachidonic acid and the metabolic syndrome in Costa Rican adults." Williams ES, Baylin A, Campos H: Clin Nutr 26:474-482, 2007 "Arachidonic acid content in adipose tissue is associated with insulin resistance in healthy children." Aldamiz-Echevarria L, Prieto JA, Andrade F, Elorz J, Sanjurjo P, Rodriguez Soriano J: J Pediatr Gastroenterol Nutr 44:77-83, 2007 "Enhanced proportion of small adipose cells in insulin-resistant vs. insulin-sensitive obese individuals implicates impaired adipogenesis." McLaughlin T, Sherman A, Tsao P, Gonzalez O, Yee G, Lamendola C, Reaven GM, Cushman SW: Diabetologia 50:1707-1715, 2007 "Anti-Inflammatory Medicine: Dietary Modulation of Eicosanoids" Inflammation Research Foundation, Marblehead, MA www.inflammationresearchfoundation.org Obesity and cancer share many similarities. They are both characterized by increased inflammation (as marked by increased macrophage concentration), seemingly uncontrolled growth, as well as metastasis to distant sites. The excess fat mass in an individual who is actively sequestering AA from the circulation represents a benign tumor because it does not compromise physiological function. This explains why approximately one-third of obese individuals are actually quite healthy. These individuals are known as the metabolically healthy obese and appear to have higher levels of the adipose-derived hormone adiponectin. "The obese without cardiometabolic risk factor clustering and the normal weight with cardiometabolic risk factor clustering: prevalence and correlates of 2 phenotypes among the US population." Wildman RP,Muntner P, Reynolds K, McGinn AP, Rajpathak S, Wylie-Rosett J, Sowers MR: (NHANES 1999-2004). Arch Intern Med 168:1617-1624, 2008 "The metabolically healthy but obese individual presents a favorable inflammation profile. " Karelis AD, Faraj M, Bastard JP, St-Pierre DH, Brochu M, Prud'homme D, Rabasa-Lhoret R. J Clin Endocrinol Metab. 90:4145-4150, 2005 "High adiponectin concentrations are associated with the metabolically healthy obese phenotype. " Aguilar-Salinas CA Garcia EG Robles L Riano D Ruiz-Gomez DG Garcia-Ulloa AC, Melgarejo MA, Zamora M, Guillen-Pineda LE, Mehta R, Canizales-Quinteros S, Tusie Luna MT, Gomez-Perez FJ: J Clin Endocrinol Metab 93:4075-4079, 2008 "Anti-Inflammatory Medicine: Dietary Modulation of Eicosanoids" Inflammation Research Foundation, Marblehead, MA www.inflammationresearchfoundation.org 
Acute pancreatitis is an inflammation of the pancreas that may lead to systemic inflammatory response syndrome and death due to multiple organ failure. "Protein phosphatases and chromatin modifying complexes in the inflammatory cascade in acute pancreatitis." Escobar J, Pereda J, Arduini A, Sandoval J, Sabater L, Aparisi L, Lopez-Rodas G, Sastre J. World J Gastrointest Pharmacol Ther. 2010 Jun 6;1(3):75-80. The relationships between pancreatic maldigestion, intestinal ecology and intestinal inflammation have not received particular attention, even if in clinical practice these mechanisms may be responsible for the low efficacy of pancreatic extracts in abolishing steatorrhea in some patients. The best treatments for pancreatic maldigestion should be re-evaluated, taking into account not only the correction of pancreatic insufficiency using pancreatic extracts and the best duodenal pH to permit optimal efficacy of these extracts, but we also need to consider other therapeutic approaches including the decontamination of intestinal lumen, supplementation of bile acids and, probably, the use of probiotics which may attenuate intestinal inflammation in chronic pancreatitis patients. "Chronic pancreatitis: maldigestion, intestinal ecology and intestinal inflammation." Pezzilli R. World J Gastroenterol. 2009 Apr 14;15(14):1673-6. 
Although replacement of dopamine can temporarily alleviate the symptoms of PD patients, it can not prevent the progression of the disease. Increasing evidence has suggested that neuroinflammation significantly contributes to the progress of PD. Therefore, anti-inflammatory therapy could represent a promising neuroprotective intervention with the potential to delay or prevent onset of the disease. "Novel anti-inflammatory and neuroprotective agents for Parkinson's disease." Lu L, Li F, Wang X. CNS Neurol Disord Drug Targets. 2010 Apr;9(2):232-40. The potential causes of PD remain uncertain, but recent studies suggest neuroinflammation and microglia activation play important roles in PD pathogenesis. "Neuroinflammation in Parkinson's disease: its role in neuronal death and implications for therapeutic intervention." Tansey MG, Goldberg MS. Neurobiol Dis. 2010 Mar;37(3):510-8. Epub 2009 Nov 10. Numerous recent findings indicate the possible involvement of an immune mechanism in the pathogenesis of neurodegeneration. The immune reaction could either act as a primary event, generating changes leading to cell death, or could be a secondary response to neuronal injury. In various neurodegenerative disorders such as Alzheimer's, Huntington's or Pick's disease, Down's syndrome, multiple sclerosis and the AIDS-dementia complex, the inflammatory pathomechanism is strongly supported by experimental and clinical studies. Such inflammatory mechanisms have also been postulated in Parkinson's disease (PD). "Inflammation and Parkinson's disease." Wersinger C, Sidhu A. Curr Drug Targets Inflamm Allergy. 2002 Sep;1(3):221-42. Inflammatory and immune, or even autoimmune, stigmata, have been described in post-mortem brains of PD patients. Although disputed in humans, a reactive astrocytosis and a lymphocytic infiltration in the SNpc have been observed in animal models of PD, which need further examination. The current knowledge on brain inflammation in humans with PD, and how inflammation and/or (auto)immune reactions within the SNpc could be linked to other pathophysiological mechanisms that have been hypothesized for the etiology of PD, such as oxidative stress, exposure to neurotoxins, and post-infectious or post-traumatic injuries. In particular, we discuss how microglial cells could be activated during the course of PD, and present a new hypothesis that PD-linked protein (alpha-synuclein, in particular) aggregates could be implicated in their activation, to induce a chronic and sustained inflammation involved in the progression, at least, of the disease. "An inflammatory pathomechanism for Parkinson's disease" Wersinger C, Sidhu A. Curr Med Chem. 2006;13(5):591-602. Most acute and chronic neurodegenerative conditions are accompanied by neuroinflammation; yet the exact nature of the inflammatory processes and whether they modify disease progression is not well understood. "Neuroinflammatory mechanisms in Parkinson's disease: potential environmental triggers, pathways, and targets for early therapeutic intervention." Tansey MG, McCoy MK, Frank-Cannon TC. Exp Neurol. 2007 Nov;208(1):1-25. Epub 2007 Jul 17. Among the pathogenic processes contributing to dopaminergic neuron (DN) death in Parkinson disease (PD), evidence points to non-cell-autonomous mechanisms, particularly chronic inflammation mounted by activated microglia. "Microglial glucocorticoid receptors play a pivotal role in regulating dopaminergic neurodegeneration in parkinsonism." Ros-Bernal F, Hunot S, Herrero MT, Parnadeau S, Corvol JC, Lu L, Alvarez-Fischer D, Carrillo-de Sauvage MA, Saurini F, Coussieu C, Kinugawa K, Prigent A, Hglinger G, Hamon M, Tronche F, Hirsch EC, Vyas S. Proc Natl Acad Sci U S A. 2011 Apr 19;108(16):6632-7. Epub 2011 Apr 5. While different mechanisms including environmental toxins and genetic factors initiate neuronal damage in the substantia nigra and striatum in PD, there is unequivocal evidence that activation of neuroinflammatory cells aggravates this neurodegenerative process. It was shown that following an acute exposure to the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and other toxins the degenerative process continues for years in absence of the toxin. Reactive microglia has been observed in the substantia nigra of patients with PD, indicating that this inflammatory process might aggravate neurodegeneration. By releasing various kinds of noxious factors such as cytokines or proinflammatory molecules microglia may damage CNS cells. The stimuli triggering microgliosis in Parkinsonian syndromes are unknown so far: However, analysis of neuronal loss in PD patients shows that it is not uniform but that neurons containing neuromelanin (NM) are predominantly involved. "Inflammation in Parkinson's diseases and other neurodegenerative diseases: cause and therapeutic implications." Wilms H, Zecca L, Rosenstiel P, Sievers J, Deuschl G, Lucius R. Curr Pharm Des. 2007;13(18):1925-8. 
Poliomyelitis, often called polio or infantile paralysis, is an acute viral infectious disease spread from person to person, primarily via the fecal-oral route. The term derives from the Greek polios, meaning "grey", myelos, referring to the "spinal cord", and the suffix -itis, which denotes inflammation. The destruction of neuronal cells produces lesions within the spinal ganglia; these may also occur in the reticular formation, vestibular nuclei, cerebellar vermis, and deep cerebellar nuclei. Inflammation associated with nerve cell destruction often alters the color and appearance of the gray matter in the spinal column, causing it to appear reddish and swollen. "Chapter 175: Enteroviruses and Reoviruses." Cohen JI (2004). In Kasper DL, Braunwald E, Fauci AS, et al. (eds.). Harrison's Principles of Internal Medicine (16th ed.). McGraw-Hill Professional. pp. 1144. ISBN 0-07-140235-7. "The Gale Encyclopedia of Neurological Disorders." Chamberlin SL, Narins B (eds.) (2005). Detroit: Thomson Gale. pp. 1859 70. ISBN 0-7876-9150-X. "Poliovirus and poliomyelitis: a tale of guts, brains, and an accidental event." Mueller S, Wimmer E, Cello J (2005).Virus Res 111 (2): 175 93. doi:10.1016/j.virusres.2005.04.008. PMID 15885840. 
In this text, an international panel of prestigious authors explore the complex relationship between inflammation, the mother, placenta and fetus. Providing comprehensive coverage by discussing both basic sciences and clinical applications, the book also ensures wide appeal by presenting a synthesis of the maternal and fetal aspects of immunological disorders in pregnancy. "Inflammation and Pregnancy." Donald M Peebles, Leslie Myatt, Informa Healthcare (September 15, 2006) ISBN: 978-1-84214-272-1 Inflammation is a process by which tissues respond to various insults. It is characterized by upregulation of chemokines, cytokines, and pattern recognition receptors that sense microbes and tissue breakdown products. During pregnancy, the balance of Th1 (cell-mediated immunity) and Th2 (humoral immunity) cytokines is characterized by an initial prevalence of Th2 cytokines, followed by a progressive shift toward Th1 predominance late in gestation, that when is abnormal, may initiate and intensify the cascade of inflammatory cytokine production involved in adverse pregnancy outcomes. "Inflammation and Pregnancy." John R. Challis, PhD, Charles J. Lockwood, MD, Leslie Myatt, PhD, Jane E. Norman, MD, Jerome F. Strauss III, MD, PhD and Felice Petraglia, MD. Reproductive Sciences February 2009 vol. 16 no. 2 206-215 doi: 10.1177/1933719108329095 The clinical relevance of histologic evidence of acute ascending intrauterine infection has been called into question by descriptions of "silent" chorioamnionitis. The described frequencies of silent chorioamnionitis in normal and abnormal pregnancies vary widely because of differences in the definition of a normal pregnancy, methods of placental examination, and pathologic criteria. Therefore, we examined placentas from 161 uncomplicated gestations for the presence and severity of acute inflammation in the amnion, chorion-decidua, chorionic plate, and umbilical cord using strict gross and microscopic protocols. Indicators of amniotic fluid infection, specifically umbilical cord inflammation, amnionitis, and inflammation within the chorionic plate were present in 0, 1.2, and 4% of the cases, respectively. Silent chorioamnionitis was rare. There was a statistical association between the presence of acute inflammation and the occurrence of labor at term. "The prevalence and distribution of acute placental inflammation in uncomplicated term pregnancies." Salafia CM, Weigl C and Silberman L. Obstetrics and Gynecology [1989, 73(3 Pt 1):383-9] Fetal cells enter the maternal circulation during pregnancy. The presence of fetal cells has been demonstrated in lesional skin of pregnant women affected with polymorphic eruptions of pregnancy. We aimed to determine in mouse models the role of maternal inflammation in attracting microchimeric cells. Using various techniques in different reporting mice, we demonstrated that maternal skin can recruit fetal endothelial cells as well as fetal leucocytes in CHR. Fetal cells may therefore participate and possibly influence maternal angiogenesis and inflammation. "Maternal skin inflammation during pregnancy recruits fetal endothelial and inflammatory cells." Nguyen, Huu S., Aractingi, S., Oster, M., Espie, M. J., Chareyre, F. and Khosrotehrani, K. 36th Annual Meeting of the European Society of Dermatology Research Meeting. 36th Annual Meeting of the European Society of Dermatology Research Meeting, Paris, (s45-s45). 7-9 September 2006. Fetal development and growth occur in a sterile amniotic cavity while first exposure to microorganisms happens at birth. However, at least 25% of all preterm births, the leading cause of perinatal morbidity and mortality worldwide, occur in mothers with microbial invasion of the amniotic cavity. Microbial attack of the fetus takes place in approximately 10% of pregnancies with intra-amniotic infection, and the human fetus is capable of deploying an inflammatory response (cellular and humoral) in the mid-trimester of pregnancy. The onset of premature labor in the context of infection is mediated by pro-inflammatory cytokines, such as interleukin (IL)-1beta and tumor necrosis factor alpha (TNF-alpha), as these cytokines are produced by intrauterine tissues in response to microbial products, can stimulate prostaglandin production, and induce labor in animals. Moreover, knockout experiments suggest that infection is less likely to lead to premature labor when the IL-1 and TNF signaling pathways are disrupted. A fetal inflammatory systemic response occurs in a fraction of fetuses exposed to microorganisms in utero, and is associated with the impending onset of labor as well as multisystem organ involvement. Neonates born with funisitis, the histologic marker of such inflammation, are at increased risk for neurologic handicap and cerebral palsy. Evidence has begun to accumulate that gene-environment interactions determine the likelihood of preterm labor and delivery and, probably, the risk of fetal injury. Fetal inflammation has emerged as a major mechanism of disease responsible for complications in the perinatal period (in utero and in the first 28 days of life), as well as in infancy. Moreover, reprogramming of the fetal immune response may predispose to diseases in adulthood. "Inflammation in pregnancy: its roles in reproductive physiology, obstetrical complications, and fetal injury." Romero R, Gotsch F, Pineles B, Kusanovic JP. Nutr Rev. 2007 Dec;65(12 Pt 2):S194-202. A new study shows that women who report high levels of stress and low social support during pregnancy are more likely to have increased immune system activity, which can trigger inflammatory responses and put them at risk for premature labor and preeclampsia. These inflammatory immune system responses involve increases in two proteins cytokines and C-reactive protein (CRP). "Psychosocial stress increases inflammatory markers and alters cytokine production across pregnancy." Coussons-Read ME, Okun ML, Nettles CD. Brain, Behavior, and Immunity, 21(3), 2007. "Stress Increases Inflammation In Pregnancy, Putting Women At Risk." Medical News Today, 11 Apr 2007 www.medicalnewstoday.com/releases/67473.php One of the most commonly cited thyroid changes during pregnancy is a slight enlargement or inflammation of the gland that mimics some of the symptoms of a goiter, which is caused by iodine deficiency. However, in developed nations, most balanced diets offer ready access to iodine, and as such, true pregnancy-related goiters are very rare. In the vast majority of pregnant women, the outcome of this inflammation is a slight, temporary enlargement of the thyroid that is usually undetectable to the naked eye. "Pregnancy and Thyroid." MedicalOnly.com 2007 www.medicalonly.com/2007/03/09/pregnancy_thyroid Efforts to improve maternal nutrition during pregnancy prompted an observational study of the occurrence of maternal iron deficiency and its laboratory diagnosis in almost 500 pregnancies. Methods: In this longitudinal study, the biochemical and haematological iron indices of women (n=492) attending a prenatal clinic in a Dublin maternity hospital were assessed at first booking (mean 15.9 weeks), and after 24 weeks, and 36 weeks of gestation. A high occurrence iron deficiency (ID) at first booking (SF<12 g/L) had increased over six-fold by 24 weeks, and all biochemical iron indices reflected progressive iron depletion right up to term. "Laboratory assessment of iron status in pregnancy." Walsh T, O'Broin SD, Cooley S, Donnelly J, Kennedy J, Harrison RF, McMahon C, Geary M. Clin Chem Lab Med. 2011 May 31. High levels of chronic inflammation increase miscarriage and pre-eclampsia. Suppression of inflammation with anti-oxidants, omega-3 oils, aspirin and heparin, improve fertility and decrease complications of pregnancy. Pre-eclampsia is a potentially dangerous increase in blood pressure and loss of protein into the urine, proteinuria. Further increase in these symptoms without prompt treatment, could result in eclampsia, seizure. Since pre-eclampsia normally develops during the third trimester, the usual treatment is induction of birth. There is increasing evidence that pre-eclampsia is brought on by increasing oxidative stress, depletion of natural anti-oxidants and depletion of omega-3 fatty acids. It appears that pre-eclampsia can be treated as an omega-3 fatty acid deficiency and inflammation. "The effect of recurrent miscarriage and infertility on the risk of pre-eclampsia." Trogstad L, Magnus P, Moffett A, Stoltenberg C. 2009. BJOG. 116(1):108-13. "Fatty acids, antioxidants, and oxidative stress in pre-eclampsia." Mehendale S, Kilari A, Dangat K, Taralekar V, Mahadik S, Joshi S. 2008. Int J Gynaecol Obstet. 100(3):234-8. Women of childbearing age are at risk of vitamin D deficiency (VDD) because of low sun exposure and low dietary intake of vitamin D. While the major, long-term risks of VDD for these women are well known (i.e., loss of bone mineral density) recent studies suggest that VDD in pregnancy may increase the risk of inflammation-related adverse events, including preeclampsia. "Inflammation and Pregnancy Outcomes in Women at Risk of Vitamin D Deficiency." Professor Dena Towner, M.D. and Bryon Jacoby, M.D. UC Davis Department of Obstetrics and Gynecology www.ucdmc.ucdavis.edu/obgyn/research/VitaminD.html The concept that pregnancy is associated with immune suppression has created a myth of pregnancy as a state of immunological weakness and, therefore, of increased susceptibility to infectious diseases. A challenging question is whether the maternal immune system is a friend or a foe of pregnancy. In this review, we discuss data associated to the role of the immune system during pregnancy. We propose a new paradigm in terms of the fetal-maternal immune interaction as well as the immunological response of the mother to microorganism. "Inflammation and pregnancy: the role of the immune system at the implantation site." Mor G, Cardenas I, Abrahams V, Guller S. Ann N Y Acad Sci. 2011 Mar;1221:80-7. doi: 10.1111/j.1749-6632.2010.05938.x. Chronic amniotic fluid inflammation may cause preterm labor, with the involvement of different mediators that produce diverse aspects of the inflammatory response. "Intrauterine inflammation and preterm delivery." Vrachnis N, Vitoratos N, Iliodromiti Z, Sifakis S, Deligeoroglou E, Creatsas G. Ann N Y Acad Sci. 2010 Sep;1205:118-22. doi: 10.1111/j.1749-6632.2010.05684.x. Obesity has reached epidemic proportions in our patients who are of childbearing age, with pregnant patients of normal weight being in the minority. The pregnancy-related complications attributable to obesity affect not only the pregnant women, but also her fetus and potentially both mother and child for their lifetimes. Pregnancy is associated with altered immunity. The physiologic state of chronic inflammation in obesity affects systemic immunity and metabolism, and may be associated with several of the complications associated with maternal obesity. The interplay between pregnancy, obesity and inflammation may have far-reaching implications for fertility, pregnancy, the fetus and neonate. "Maternal obesity: the interplay between inflammation, mother and fetus." M Schmatz, J Madan, T Marino and J Davis. Journal of Perinatology 30, 441-446 (July 2010) | doi:10.1038/jp.2009.182 Fetal development and growth occur in a sterile amniotic cavity while first exposure to microorganisms happens at birth. However, at least 25% of all preterm births, the leading cause of perinatal morbidity and mortality worldwide, occur in mothers with microbial invasion of the amniotic cavity. Microbial attack of the fetus takes place in approximately 10% of pregnancies with intra-amniotic infection, and the human fetus is capable of deploying an inflammatory response (cellular and humoral) in the mid-trimester of pregnancy. Fetal inflammation has emerged as a major mechanism of disease responsible for complications in the perinatal period (in utero and in the first 28 days of life), as well as in infancy. "Inflammation in pregnancy: its roles in reproductive physiology, obstetrical complications, and fetal injury." Romero Roberto; Gotsch Francesca; Pineles Beth; Kusanovic Juan Pedro. Nutrition reviews 2007;65(12 Pt 2):S194-202. 2007: About 11,000 women under the age of 40 are diagnosed with breast cancer in the United States each year. Of that number, about 50 percent had a baby in the six years prior to diagnosis. Those who are diagnosed within two years of giving birth have a 40 percent five-year survival rate, compared to an 70 percent five-year survival rate for women who are 15 years post-delivery at diagnosis. After several years of looking at inflammation related to weaning as the cause of poorer prognosis, they now think the condition may also be related to the normal pregnancy immune response that keeps a woman's body from rejecting the developing fetus. They will be testing this hypothesis in the first part of the project by comparing inflammation and immune response markers in women under age 50 who have and have not been diagnosed with breast cancer within six years of giving birth. "We're beginning to realize that some of same immune mechanisms that are suppressed during pregnancy are the same mechanisms that cancer cells use to escape the immune system," she says. "Borges receives $246,667 to study inflammation in pregnancy associated breast cancer." Lynn Clark, University of Colorado Cancer Center (2008). 
Epidemiological studies have shown that patients with psoriasis have a higher risk of developing certain metabolic disorders, particularly obesity. Psoriasis and obesity are linked through a common pathophysiological mechanism of chronic low-grade inflammation. "Psoriasis and Obesity: A Review and Practical Recommendations." Faras MM, Serrano V, de la Cruz C. Actas Dermosifiliogr. 2011 May 19. FDG-PET/CT identified numerous foci of inflammation in 6 patients with psoriasis within the skin, liver, joints, tendons, and aorta. Inflammation in the joints was observed in a patient with psoriatic arthritis as well as in 1 patient with no history of joint disease or joint symptoms. In a nested case-control study, FDG-PET/CT imaging demonstrated increased vascular inflammation in multiple segments of the aorta compared with controls. These findings persisted after adjustment for traditional cardiovascular risk factors in multivariate analysis (mean B = 0.33; P < .001). Patients with psoriasis further demonstrated increased hepatic inflammation after adjusting for cardiovascular risk factors (B = 0.18; P < .001), but the association was no longer significant when adjusted for alcohol intake (B = -0.25; P = .07). Conclusion FDG-PET/CT is a sensitive tool for identifying inflammation and can be used to identify clinically observed inflammation in the skin and subclinical inflammation in the blood vessels, joints, and liver of patients with psoriasis. "Systemic and Vascular Inflammation in Patients With Moderate to Severe Psoriasis as Measured by [18F]-Fluorodeoxyglucose Positron Emission Tomography-Computed Tomography (FDG-PET/CT): A Pilot Study." Mehta NN, Yu Y, Saboury B, Foroughi N, Krishnamoorthy P, Raper A, Baer A, Antigua J, Van Voorhees AS, Torigian DA, Alavi A, Gelfand JM. Arch Dermatol. 2011 May 16. 
Pulmonary hypertension (PH) is a serious disorder with high morbidity and mortality rate. Evidence is accumulating to suggest that inflammation plays a significant role in the pathogenesis of PH. Endothelial cells play an important role in inflammation and immune reactions, and inflammatory cytokines cause endothelial dysfunction. "Inflammation and Pulmonary Hypertension." Mathew, Rajamma MD, Cardiology in Review: March/April 2010 - Volume 18 - Issue 2 - pp 67-72 doi: 10.1097/CRD.0b013e3181cd612f Inflammatory mechanisms appear to play a significant role in some types of pulmonary hypertension (PH), including monocrotaline-induced PH in rats and pulmonary arterial hypertension of various origins in humans, such as connective tissue diseases (scleroderma, systemic lupus erythematosus, mixed connective disease), human immunodeficiency virus infection, or plasma cell dyscrasia with polyneuropathy, organomegaly, endocrinopathy, monoclonal (M) protein and skin changes (POEMS) syndrome. "Inflammation in pulmonary arterial hypertension." P. Dorfmuller, F. Perros, K. Balabanian and M. Humbert. ERJ August 1, 2003 vol. 22 no. 2 358-363 doi: 10.1183/09031936.03.00038903 Inflammation plays a significant role in various types of human PH such as IPAH and PAH associated with connective tissue diseases and HIV infection, and in experimental animal models (e.g., monocrotaline (MCT)-induced PH). A subset of PAH patients have circulating autoantibodies, including antinuclear antibodies [2] and elevated circulating levels of the proinflammatory cytokines interleukin-1 (IL-1) and IL-6. [3] While there are serologic and pathologic features suggestive of inflammation in both IPAH and PAH related to connective tissue diseases, it is likely that inflammatory pathways and autoimmunity are more pronounced in connective tissue diseases and may explain survival discrepancies and differential response to therapy between the two syndromes. "Role of inflammation in pulmonary arterial hypertension." Paul M Hassoun PVRI Review 2010, Volume : 2, Issue : 1, Page : 2-4 "Autoantibodies in patients with primary pulmonary hypertension: Association with anti-Ku." Isern RA, Yaneva M, Weiner E, Parke A, Rothfield N, Dantzker D, et al. Am J Med 1992;93:307-12. "Increased interleukin-1 and interleukin-6 serum concentrations in severe primary pulmonary hypertension."Humbert M, Monti G, Brenot F, Sitbon O, Portier A, Grangeot-Keros L, et al. Am J Respir Crit Care Med 1995;151:1628-31. "Connective tissue disease associated pulmonary arterial hypertension in the modern treatment era."Condliffe R, Kiely DG, Peacock AJ, Corris PA, Gibbs JS, Vrapi F, et al. Am J Respir Crit Care Med 2009;179:151-7. "Clinical differences between idiopathic and scleroderma-related pulmonary hypertension."Fisher MR, Mathai SC, Champion HC, Girgis RE, Housten-Harris T, Hummers L, et al. Arthritis Rheum 2006;54:3043-50. 
Scleroderma is a chronic systemic autoimmune disease (primarily of the skin) characterized by fibrosis (or hardening), vascular alterations, and autoantibodies. It affects the small blood vessels (arterioles) in all organs. First, the endothelial cells of the arteriole die off, along with smooth muscle cells, by a process of apoptosis. They are replaced by collagen and other fibrous material. Inflammatory cells, particularly CD4+ helper T cells, infiltrate the arteriole, and cause further damage. "Scleroderma." Gabrielli A, Avvedimento EV, Krieg T (May 2009). N. Engl. J. Med. 360 (19): 1989 2003. doi:10.1056/NEJMra0806188. PMID 19420368. "Scleroderma." Wikipedia en.wikipedia.org/wiki/Scleroderma Localized scleroderma (LS) is a disfiguring autoimmune disease of the skin and underlying tissue that mainly affects the pediatric population. Inflammation of the tissue leads to fibrosis and atrophy, causing physical and psychological disability that can continue throughout childhood into adulthood. "Cytokine profiles in localized scleroderma and relationship to clinical features." Kurzinski K, Torok KS. Cytokine. 2011 Apr 30. 
Small bowel bacterial overgrowth syndrome (SBBOS), or small intestinal bacterial overgrowth (SIBO), also termed bacterial overgrowth; is a disorder of excessive bacterial growth in the small intestine. Many of the symptoms are due to malabsorption of nutrients due to the effects of bacteria which either metabolize nutrients or cause inflammation of the small bowel impairing absorption. There are 500-1000 different species of bacteria that reside in the bowel. However, if the flora of the small bowel is altered, inflammation or altered digestion can occur, leading to symptoms. Various mechanisms are involved in the development of diarrhea in bacterial overgrowth. First, the excessive bacterial concentrations can cause direct inflammation of the small bowel cells, leading to an inflammatory diarrhea. "Small intestinal bacterial overgrowth: roles of antibiotics, prebiotics, and probiotics." Quigley E, Quera R (2006). Gastroenterology 130 (2 Suppl 1): S78 90. doi:10.1053/j.gastro.2005.11.046. PMID 16473077. "Small bowel bacterial overgrowth is a common cause of chronic diarrhea." Teo M, Chung S, Chitti L, Tran C, Kritas S, Butler R, Cummins A (2004). J Gastroenterol Hepatol 19 (8): 904 9. doi:10.1111/j.1440-1746.2004.03376.x. PMID 15242494. "Bacterial overgrowth." Kirsch M (1990). Am J Gastroenterol 85 (3): 231 7. PMID 2178395. "Microflora of the gastrointestinal tract: a review." Hao W, Lee Y (2004). Methods Mol Biol 268: 491 502. doi:10.1385/1-59259-766-1:491. PMID 15156063. "Small bowel bacterial overgrowth syndrome." Wikipedia en.wikipedia.org/wiki/Small_bowel_bacterial_overgrowth_syndrome Hepatobiliary inflammation and other extraintestinal manifestations accompany certain intestinal disorders, perhaps because of proliferation or enhanced transport of luminal bacteria or their phlogistic cell-wall components. Using jejunal self-filling blind loops to create small bowel bacterial overgrowth, we compared biochemical and histological evidence of hepatic inflammation in 3 rat strains chosen for their variable inflammatory responses to bacterial cell wall polymers. Our results show that experimental small bowel bacterial overgrowth causes significant hepatic inflammation leading to fibrosis in susceptible rat strains. Caloric deprivation and hepatic bacterial invasion are not etiologically responsible. We suggest that bacterial cell wall polymers or other bacterial toxins from the blind loop cause hepatic lesions in genetically susceptible hosts. "Hepatic inflammation in rats with experimental small intestinal bacterial overgrowth." Lichtman SN, Sartor RB, Keku J, Schwab JH. Gastroenterology. 1990 Feb;98(2):414-23. 
Sjogren's syndrome "Mikulicz disease" and "Sicca syndrome" is a systemic autoimmune disease in which immune cells attack and destroy the exocrine glands that produce tears and saliva. A slit-lamp examination is done to look for dryness on the surface of the eye. Salivary gland function can be tested by collecting saliva and determining the amount produced in a five minute period. A lip biopsy can reveal lymphocytes clustered around salivary glands, and damage to these glands due to inflammation. Medication is available by prescription to help treat chronic dry eye by suppressing the inflammation that disrupts tear secretion. "Dermatology: 2-Volume Set." Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). St. Louis: Mosby. pp. 602 3. ISBN 1-4160-2999-0. "Biomarker profiles in serum and saliva of experimental Sjogren's syndrome: associations with specific autoimmune manifestations." Delaleu N, Immervoll H, Cornelius J, Jonsson R (2008). Arthritis Res. Ther. 10 (1): R22. doi:10.1186/ar2375. PMC 2374466. PMID 18289371. http://arthritis-research.com/content/10/1/R22. "Sjogren's syndrome." Wikipedia en.wikipedia.org/wiki/Sjogren's_syndrome Systemic inflammatory diseases are associated with keratitis. In addition to the much less frequently occurring non-ulcerative keratitis, ulcerative inflammation of the corneal periphery is common in systemic inflammatory diseases. Significant systemic inflammatory diseases in this context are autoimmune connective tissue diseases (including rheumatoid arthritis, systemic lupus erythematosus or primary vasculitides such as polyarteritis nodosa or Wegener's granulomatosis), systemic autoimmune dermatological disorders (such as the cicatrising pemphigoid or Stevens-Johnson syndrome) and autoimmune diseases of the lacrimal system (such as the lacrimal gland involvement in primary Sjogren's syndrome or in graft-versus-host disease). "Inflammation of the Eye in Systemic Inflammatory Disorders: Keratitis." Bachmann B, Jacobi C, Cursiefen C. Klin Monbl Augenheilkd. 2011 May;228(5):413-418. Epub 2011 Apr 29. 
Sleep apnea is a sleep disorder characterized by abnormal pauses in breathing or instances of abnormally low breathing, during sleep. Each pause in breathing, called an apnea, can last from a few seconds to minutes, and may occur 5 to 30 times or more an hour. Similarly, each abnormally low breathing event is called a hypopnea. Sleep apnea is diagnosed with an overnight sleep test called a polysomnogram, or "sleep study". Indirect evidence implicates endothelial dysfunction in the pathogenesis of vascular diseases associated with obstructive sleep apnea (OSA). We investigated directly whether dysfunction and inflammation occur in vivo in the vascular endothelium of patients with OSA. The effects of continuous positive airway pressure (CPAP) therapy on endothelial function and repair capacity were assessed. OSA directly affects the vascular endothelium by promoting inflammation and oxidative stress while decreasing NO availability and repair capacity. Effective CPAP therapy is associated with the reversal of these alterations. "Inflammation, Oxidative Stress, and Repair Capacity of the Vascular Endothelium in Obstructive Sleep Apnea." Sanja Jelic MD*, Margherita Padeletti MD, Steven M. Kawut MD, MS, Christopher Higgins MD, Stephen M. Canfield MD, Duygu Onat PhD, Paolo C. Colombo MD, Robert C. Basner MD, Phillip Factor DO, and Thierry H. LeJemtel MD. Circulation: The Journal of the American Heart Association (14, 2008) doi: 10.1161/CIRCULATIONAHA.107.741512 "Sleep Apnea: What Is Sleep Apnea" NHLBI: Health Information for the Public. U.S. Department of Health and Human Services. 2009-05. www.nhlbi.nih.gov/health/dci/Diseases/SleepApnea/SleepApnea_WhatIs.html. Endothelial dysfunction, resulting from IH and as a key early event in atherosclerosis, was demonstrated repeatedly in patients with Obstructive sleep apnea and in animal models of IH, providing an important mechanistic link between the acute cyclical IH during sleep and the increased prevalence of chronic vascular diseases. From this work, we conclude that IH from Obstructive sleep apnea may result in endothelial dysfunction, as a potential promoter of atherosclerosis, through nitric oxide unavailability, oxidative stress and inflammation, cell apoptosis, the crosstalk between endothelial cells and circulating inflammatory cells, microparticles, and damage repairing process. "Endothelial mechanisms of endothelial dysfunction in patients with obstructive sleep apnea." Feng J, Zhang D, Chen B. Sleep Breath. 2011 Apr 10. Obstructive sleep apnoea syndrome (OSAS) is a highly prevalent disease and associated with cardiovascular morbidity and mortality. The pathogenesis of cardiovascular complications in OSAS is incompletely understood but a multifactorial etiology is likely. There is emerging evidence that inflammatory processes leading to endothelial dysfunction play a pivotal role. "Obstructive sleep apnea and inflammation: Relationship to cardiovascular co-morbidity." Kent BD, Ryan S, McNicholas WT. Respir Physiol Neurobiol. 2011 Mar 23. 
Myelitis is a disease involving inflammation of the spinal cord, which disrupts central nervous system functions linking the brain and limbs. The name is derived from Greek myelos referring to the "spinal cord", and the suffix -itis, which denotes inflammation. "Myelitis." Wikipedia en.wikipedia.org/wiki/Myelitis "The Gale Encyclopedia of Neurological Disorders." Chamberlin SL, Narins B (eds.) (2005). Detroit: Thomson Gale. pp. 1859 70. ISBN 0-7876-9150-X. Inflammation, which is known to be detrimental to the neurologic outcome during the acute phase after an ischemic stroke, provides a potential target for preventive or therapeutic approach for spinal cord ischemia-reperfusion injury. Treatment with TMP exerted a neuroprotective effect against spinal cord ischemia-reperfusion injury. The anti-inflammatory effect was believed to be one of the contributing mechanisms. "Tetramethylpyrazine protects spinal cord and reduces inflammation in a rat model of spinal cord ischemia-reperfusion injury." Fan L, Wang K, Shi Z, Die J, Wang C, Dang X. J Vasc Surg. 2011 Mar 30. Spinal cord injuries are described at various levels of "incomplete", which can vary from having no effect on the patient to a "complete" injury which means a total loss of function. Treatment of spinal cord injuries starts with restraining the spine and controlling inflammation to prevent further damage. Inflammation can cause further damage to the spinal cord, and patients are sometimes treated with a corticosteroid drug such as methylprednisolone to reduce swelling. "Spinal Cord Injury." en.wikipedia.org/wiki/Spinal_cord_injury "The trauma manual." Andrew B., MD Peitzman; Andrew B. Peitzman; Michael, MD Sabom; Donald M., MD Yearly; Timothy C., MD Fabian (2002). Hagerstwon, MD: Lippincott Williams & Wilkins. pp. 140 56. ISBN 0-7817-2641-7. The molecular basis of spinal cord inflammation draws from a vast arsenal of known immunologic molecules, including cytokines and chemokines, as well as growth factors, trophic factors, and other agents. Cytokines, of which there are about 60, regulate cell-cell communication between immune cells. They are small proteins that produce local and transient effects. Chemokines are chemotactic molecules that attract immune cells, helping them to "home" to sites of inflammation. Frequently, the cells producing these regulatory molecules also bear receptors for them, participating in a complex network of self-regulating and local interactions that orchestrates the proliferation of immune cells and then the subsequent decline of immune activity. A central theme is to determine in what ways the activity of inflammatory cells is good for neural recovery and regeneration, and in what ways deleterious. Gennadij Raivich presented evidence that the immediate inflammatory response in the CNS seems better suited to provide immune surveillance, to fight possible infection, and to clean up debris rather than to help the repair process. Quiescent microglia normally express few of the receptors to molecules released by the immune system, but move to an "alert" phase with injury, producing more of these receptors, dividing and "homing" to the damaged cells. The cell debris then triggers their transformation into macrophage-like cells: they engulf cell debris, and begin to produce pro-inflammatory cytokines and factors, starting a cascade of action by stimulating and recruiting other bystander microglia. Injury also stimulates resting astrocytes to express cytokines, cell adhesion molecules, trophic factors and glial fibrillary acidic protein (GFAP), a hallmark of injury and a component of gliotic scars in the adult nervous system. If the inflammatory response is deleterious to recovery, one approach might be to eliminate the immune cells that mediate this response. "Role of the Immune System in Spinal Cord Injury." National Institute of Neurological Disorders and Stroke (2011) www.ninds.nih.gov/news_and_events/proceedings/immunesciwkshp.htm Hyperalgesia is an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves. Temporary increased sensitivity to pain also occurs as part of sickness behavior, the evolved response to infection. Hyperalgesia is induced by platelet-activating factor (PAF) which comes about in an inflammatory or an allergic response. This seems to occur via immune cells interacting with the peripheral nervous system and releasing pain-producing chemicals (cytokines and chemokines). "Biological basis of the behavior of sick animals." Hart BL (1988). Neurosci Biobehav Rev 12 (2): 123 37. doi:10.1016/S0149-7634(88)80004-6. PMID 3050629. http://linkinghub.elsevier.com/retrieve/pii/S0149-7634(88)80004-6. "Role of the immune system in chronic pain." Marchand F, Perretti M, McMahon SB (July 2005). Nat. Rev. Neurosci. 6 (7): 521 32. doi:10.1038/nrn1700. PMID 15995723. "Hyperalgesia." Wikipedia en.wikipedia.org/wiki/Hyperalgesia 
A recent study published in the European Heart Journal reports that respiratory infections can increase the risk of stroke, and heart attack. The study reports that the risk of stroke is doubled within one week of a respiratory infection, and stays elevated for up to one month. These results are reminiscent of data published almost 10 years ago that respiratory tract infections increase the risk of heart attacks. "Yet One More Link Between Inflammation and Stroke: Respiratory Infections Increase The Risk of Stroke." Jose Vega M.D., Ph.D., About.com Guide stroke.about.com/b/2007/12/09/yet-one-more-link-between-inflammation-and-stroke-respiratory-infections-increase-the-risk-of-stroke.htm "Recent respiratory infection and risk of cardiovascular disease: case-control study through a general practice database." Tim C. Clayton, Mary Thompson and Tom W. Meade. The European Society of Cardiology. (2008) Systemic inflammatory events, such as infection, increase the risk of stroke and are associated with worse outcome, but the mediators of this clinically important effect are unknown. "Systemic Inflammation Alters the Kinetics of Cerebrovascular Tight Junction Disruption after Experimental Stroke in Mice." Barry W. McColl, Nancy J. Rothwell and Stuart M. Allan. J. Neurosci. (2008) 28(38): 9451-9462 Experimental evidence indicates that interleukin-10 (IL-10) deficiency is associated with the development of cardiovascular and cerebrovascular disease. We analyzed the relation between low IL-10 production levels, history of stroke, and incident fatal stroke. Our data support the hypothesis that subjects with low IL-10 production levels have an increased risk of stroke. "Inflammation and stroke: the Leiden 85-Plus Study." van Exel E, Gussekloo J, de Craen AJ, Bootsma-van der Wiel A, Frolich M, Westendorp RG. Stroke. 2002 Apr;33(4):1135-8. The incidence of infection among stroke patients is alarmingly high and both acute and delayed infections increase morbidity and mortality. Experimental studies support the acute clinical data, but little attention has focused on delayed systemic infections. Here, we investigated the effects of prolonged systemic inflammation either before or 24-h after ischemia. Our findings, together with corroborative clinical data, emphasize the importance of early intervention to counteract the deleterious consequences of stroke-associated inflammation and infection. "Prolonged, 24-h delayed peripheral inflammation increases short- and long-term functional impairment and histopathological damage after focal ischemia in the rat." Langdon KD, Maclellan CL, Corbett D. J Cereb Blood Flow Metab. 2010 Aug;30(8):1450-9. Epub 2010 Mar 24. 
Post-infectious autoimmunity has been implicated in pathogenesis of Tourette's syndrome (TS) but no evidence of inflammation in central nervous system has been reported yet. We evaluated the expression of genes encoding selected inflammatory factors in post-mortem specimen of adult TS patients. Elevated expression of MCP-1 and IL-2 supports the possibility of chronic inflammatory processes in the basal ganglia. Replication of elevated expression of PTPR-N in TS specimen suggests that pathway(s) involving this molecule may be important in TS pathogenesis. "Elevated expression of MCP-1, IL-2 and PTPR-N in basal ganglia of Tourette syndrome cases." Morer A, Chae W, Henegariu O, Bothwell AL, Leckman JF, Kawikova I. Brain Behav Immun. 2010 Oct;24(7):1069-73. Epub 2010 Mar 1. Post-streptococcal autoimmune inflammation of basal ganglia was suggested to be an etiological factor in some cases of Tourette syndrome (TS). Since regulatory T (T reg) cells play a major role in preventing autoimmunity, we hypothesized that a defect in T reg cells may be present in children with TS. We also postulated that group A beta hemolytic streptococcal infections could promote autoimmune responses by releasing exotoxins (streptococcal pyrogenic exotoxins [SPE]). Our data supports our hypothesis that at least some TS patients may have a decreased capacity to inhibit autoreactive lymphocytes through a deficit in T reg cells. Interactions of host T cell immunity and microbial factors may also contribute to the pathogenesis of TS. "Decreased numbers of regulatory T cells suggest impaired immune tolerance in children with tourette syndrome: a preliminary study." Kawikova I, Leckman JF, Kronig H, Katsovich L, Bessen DE, Ghebremichael M, Bothwell AL. Biol Psychiatry. 2007 Feb 1;61(3):273-8. Epub 2006 Sep 25. Our results provide initial evidence for a role of adhesion molecules and systemic inflammation in TS, and support the hypothesis of an ongoing immune-mediated process in this condition. "Soluble adhesion molecules in Gilles de la Tourette's syndrome." Martino D, Church AJ, Defazio G, Dale RC, Quinn NP, Robertson MM, Livrea P, Orth M, Giovannoni G. J Neurol Sci. 2005 Jul 15;234(1-2):79-85. D8/17, an alloantigen found on B lymphocytes, has been reported to be elevated in patients susceptible to rheumatic fever and may be associated with autoimmune types of neuropsychiatric disorders. The pediatric-autoimmune-neuropsychiatric-disorders-associated-with-streptococci model is a putative model of pathogenesis for a group of children whose symptoms of obsessive-compulsive disorder and Tourette's disorder (TD) are abrupt and may be triggered by an infection with group A streptococci. The percentage of CD19-positive B cells was significantly elevated in ARF and TD patients, as well as group A streptococcal pharyngitis patients, suggesting a role for inflammation and/or autoimmunity in the pathogenesis of these disorders. "D8/17 and CD19 expression on lymphocytes of patients with acute rheumatic fever and Tourette's disorder." Weisz JL, McMahon WM, Moore JC, Augustine NH, Bohnsack JF, Bale JF, Johnson MB, Morgan JF, Jensen J, Tani LY, Veasy LG, Hill HR. Clin Diagn Lab Immunol. 2004 Mar;11(2):330-6. 
Tuberculosis (TB) experts at Johns Hopkins have evidence from a four-year series of experiments in mice that anti-inflammatory drugs could eventually prove effective in treating the highly contagious lung disease, adding to current antibiotic therapies. The Johns Hopkins scientists are planning further experiments in animals infected with TB to find out if any of the already-approved anti-inflammatory drugs -- phosphodiesterase (PDE5A) inhibitors, such as sildenafil citrate (Viagra) and adenylate cyclase (AC) inhibitors would work. The new study results, to be reported in the July 2 issue of Nature, not only offer promise of a complementary or alternative therapy to antibiotics, but also open the door to vaccines designed to block the TB bacterium's inflammatory chemical pathways, the researchers say. The disease, caused by Mycobacterium tuberculosis, each year infects nearly 9 million people worldwide, and kills 1.7 million. The research team bases its claim on their recent studies in mice showing precisely how disease-causing TB bacteria provoke an inflammatory response in immune system cells and surrounding lung tissue, and that blocking the action of a key inflammation-triggering enzyme, a type of adenylate cyclase, stalled TB disease. The scientists say their findings are believed to be the first and most detailed explanation of how the invading bacterium evades the immune system and instead is protected by it, thus fostering infection. "Traditional approaches for treating TB have focused on using antibiotics to directly target and kill the bacterium after infection, eventually ridding it from the body, whereas our results suggest a new route to interrupt post-infection inflammation and disease progression, thus hindering bacterial spread within tissues," says study senior investigator and infectious disease specialist William Bishai, M.D., Ph.D. The new study showed how the highly contagious bacterium evades macrophage immune system cells meant to destroy it, by spiking production within the infected cells of inflammation-triggering chemicals, such as cyclic-adenosine monophosphate (cAMP) and tumor necrosis factor-alpha. Production of TNF-alpha is largely stimulated by cAMP, which is secreted into infected cells by the bacterium, and TNF-alpha signals other immune system cells to attack and isolate infected cells, a key part of inflammation. "Fighting tuberculosis with anti-inflammatory drugs shown possible in animal studies." Johns Hopkins University www.hopkinsmedicine.org/news/media/releases/Fighting_Tuberculosis_With_AntiInflammatory_Drugs_Shown_Possible_in_Animal_Studies (June 2009) When Mycobacterium tuberculosis infects humans, about 20% of those infected actually develop tuberculosis (TB). In Japan, the incidence of TB in 2008 was 24,760 cases (19.4/100,000 persons) and the rate has been decreasing gradually, but is still higher than in the USA, Holland, and Belgium, for example. Histologically, tuberculosis displays exudative inflammation, proliferative inflammation and productive inflammation depending on the time course. In productive inflammation, granulomatous lesions with necrotic centers are formed. The typical granulomas consist of epithelioid macrophages, Langhans' multinucleated giant cells, lymphocytes and fibroblasts, and the process of their formation involves many cytokines, chemokines and transcription factors. "Why does tuberculosis lead to specific inflammation?" Sugawara I. Nihon Hansenbyo Gakkai Zasshi. 2009 Sep;78(3):263-9. Tuberculosis is the infectious disease caused by Mycobacterium tuberculosis. It is characterized by immunologically driven necrotizing granulomatous inflammation primarily involving the lung, but less commonly also affecting lymph nodes, bones, central nervous system, gut and genitourinary system. Clinical effects are related to acute-onchronic inflammation (e.g. cough, breathlessness), to ongoing tissue destruction (e.g. haemoptysis), to the resultant scarring (e.g. urinary tract obstruction) and to the prominent systemic effects of inflammation (e.g. fever, anorexia, weight loss, anaemia of chronic disease and amyloidosis). The prominent weight loss and wasting associated with tuberculosis gave rise to the old term 'consumption', as patients appeared to be consumed by the illness. "Inflammation: Chronic." Encyclopedia of Life Sciences, 2001 Nature Publishing Group www.els.net |
Copyright © 2024 Big Meteor Publishing e-mail Restless Legs Remedy Phone: 1-613-596-4996 (Eastern Time Zone UTC/GMT -5 hours) 1203 Stanton Rd. Ottawa, Ontario K2C 3C9 Canada |