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ibs and immune system

1066 Views 7 Replies 5 Participants Last post by  floridian2
hi i have had ibs 4 about 6 months, and 4 6 months i have had colds sore throats just feeling unwell.i have had blood tests and all is normall i have an anxiety and dep problem and taking aropax 4 that.i am having enough of a problem with the ibs ,but colds in the summer is not normall 4 me.dose ibs lower the immune system?.the doctor said gladular fever may have been the problem but could not be positive and 6 months is along time 4 gf. any feedback would be good thanks
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Interferon and other immune hormones can cause anxiety and depression. If you have had an ongoing infection, these would be elevated as a natural response of the body in fighting whatever was plaguing you. I don't know that this is THE cause, but it could be contributing to your problems.
quote: Anyway, I would think the fact that IBS is categorized as functional is enough to show that there has been no observable link between IBS and the immune system. I am no expert, but I don't even see how the two could be related.
"Post-infective IBS" is a real diagnosis. Most of the time, most people have an infection, get over it, and go back to normal. In some cases, the infection can trigger changes in the body's immune system that persists for a long time. These changes can cause inflammation and a variety of disturbances across the body. The first abstract below gives an overview of post-infective IBS; the second notes high levels of IL-1B in people with post-infective IBS. The third shows how fish oils can reduce the post-infective syndrome.
quote: Rev Gastroenterol Mex. 2003 Jan-Mar;68(1):55-61. Related Articles, Links[Post-infectious irritable bowel syndrome. A review based on current evidence] [Article in Spanish] Gomez-Escudero O, Schmulson-Wasserman MJ, Valdovinos-Diaz MA. Departamento de Gastroenterologia, Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Vasco de Quiroga 15, Tlalpan, C.P. 14000 Mexico, D.F. INTRODUCTION: Pathophysiology of irritable bowel syndrome (IBS) is multifactorial. Recent investigations have associated episodes of infectious gastroenteritis with development of IBS. This condition is named post-infectious IBS (PI-IBS). The role of inflammation-infection in IBS pathogenesis is not well understood. AIM: To review published scientific evidence on PI-IBS regarding risk factors, causal agents, histopathological changes, and treatment. MATERIALS AND METHODS: An electronic search in MEDLINE and abstracts presented at national and international GI meetings was performed, looking for information published in the past 50 years including animal studies, cohort studies, case-control studies, and series of cases and case reports, using the key words post-infectious enteritis, post-dysenteric or post-infectious irritable bowel syndrome (PI-IBS), and post-infectious colitis. RESULTS: Fifty one papers were included. These studies were classified according to pathophysiologic mechanisms, infectious agents involved, animal or human studies, and treatment. CONCLUSIONS: Current evidence shows a strong association between colonic infection and inflammation with development of IBS. Approximately 25% of patients with IBS have a history of infectious enteritis. Microbial agents related with PI-IBS include bacteria (Campylobacter, Salmonella) and parasites (Trichinella spiralis). Increased number of enteroendocrine cells, CD3 lymphocytes and mast cells within the colonic muscle wall, release of pro-inflammatory substances, and increased number of inflammatory cells with intestinal nervous endings are the most common histopathologic findings. Patients developing PI-IBS have a higher frequency of psychological disorders and stressful events prior to the gastroenteritis episode. Therapeutic interventions with steroids, COX-2 inhibitors, antibiotics and probiotics require further investigation.
quote: Gut. 2003 Apr;52(4):523-6. Related Increased rectal mucosal expression of interleukin 1beta in recently acquired post-infectious irritable bowel syndrome.Gwee KA, Collins SM, Read NW, Rajnakova A, Deng Y, Graham JC, McKendrick MW, Moochhala SM.Department of Medicine, National University Hospital, Singapore. Background and aims: Chronic bowel disturbances resembling irritable bowel syndrome (IBS) develop in approximately 25% of patients after an episode of infectious diarrhoea. Although we have previously shown that psychosocial factors operating at the time of, or prior to, the acute illness appear to predict the development of post-infectious IBS (PI-IBS), our finding of an increased inflammatory cell number in the rectum persisting for at least three months after the acute infection suggested that there is also an organic component involved in the development of PI-IBS. To evaluate this further, we measured expressions of interleukin 1beta (IL-1beta) and its receptor antagonist (IL-1ra) in these patients to provide additional evidence that the pathogenesis of PI-IBS is underpinned by an inflammatory process. METHODS: Sequential rectal biopsy samples were prospectively obtained during and three months after acute gastroenteritis, from eight patients who developed post-infectious IBS (INF-IBS) and seven patients who returned to normal bowel habits after acute gastroenteritis (infection controls, INF-CON). Eighteen healthy volunteers who had not suffered from gastroenteritis in the preceding two years served as normal controls (NOR-CON). IL-1beta and IL-1ra gene expressions were assayed by reverse transcriptase-polymerase chain reaction, and their levels of expression were quantitated by optical densitometry after electrophoresis on agarose gel. RESULTS: INF-IBS patients exhibited significantly greater expression of IL-1beta mRNA in rectal biopsies than INF-CON patients both during and three months after acute gastroenteritis. Moreover, IL-1beta mRNA expression had increased in biopsies taken from INF-IBS patients at three months after the acute infection but no consistent change was observed in INF-CON patients. IL-1beta mRNA expression of INF-IBS patients at three months post gastroenteritis was significantly greater than NOR-CON whereas that of INF-CON patients was not significantly different from NOR-CON. Despite these differential changes in IL-1beta mRNA expression, no significant changes were observed in IL-1ra mRNA expression among the three groups. CONCLUSIONS: These findings indicate that those patients who develop IBS post infection exhibit greater IL-1beta mRNA expression, both during and after the infection, compared with individuals who do not develop PI-IBS. We conclude that such patients may be susceptible to inflammatory stimuli, and that inflammation may play a role in the pathogenesis of PI-IBS.
quote: J Lipid Res. 2003 Oct;44(10):1984-91. Epub 2003 Jul 01. Related Articles, Links Click here to read Effects of dietary n-3 or n-6 fatty acids on interleukin-1beta-induced anxiety, stress, and inflammatory responses in rats. Song C, Li X, Leonard BE, Horrobin DF. Department of Psychiatry, University of British Columbia, Canada. The present study demonstrated that an omega (n)-3 fatty acid, ethyl-eicosapentaenoic acid (ethyl-EPA), supplemented diet significantly attenuated the stress/anxiety behavior of rats in the "open field" and elevated plus maze, which was induced by subchronic intracerebroventricular administration of proinflammatory cytokine interleukin (IL)-1beta. Ethyl-EPA also reduced the rise in serum corticosterone induced by IL-1. The n-6 fatty acid ethyl-gamma-linolenic acid (ethyl-GLA) had little effect on the IL-1-induced changes in behavior and the corticosterone concentration. Following IL-1beta administration, ethyl-EPA reduced the elevated prostaglandin (PG) E2 secretion and increased the secretion of antiinflammatory cytokine IL-10 from whole blood cells. Ethyl-GLA showed a similar antiinflammatory effect to ethyl-EPA. By contrast, n-6 fatty acid arachidonic acid (AA) had no effect on the behavior, immune, and endocrine changes induced by IL-1. AA alone enhanced the basal inflammatory response, raised serum corticosterone concentrations, and induced anxiety behavior in the elevated plus maze. The reduced growth rates of rats following the administration of IL-1 was attenuated by ethyl-EPA, and to a greater extent by ethyl-EPA plus ethyl-GLA, but not by AA alone or in combination with ethyl-EPA. Thus, ethyl-EPA would appear to antagonise the endocrine, immune, and behavioral effects of subchronic IL-1 administration. Ethyl-GLA only antagonised IL-1-induced inflammatory changes, whereas AA caused an increase in the secretion of corticosterone and PGE2, and induced anxiety-like behavior without enhancing the effects of IL-1.
There is two way feedback between the brain and the immune system. Psychological stress increases cortisol and other hormones that supress the immune system. Benzo tranquilizers have an immediate beneficial effect in breaking the cycle, while SSRIs take longer, and can actually increase anxiety in the short run. For some people, a med for the brain is enough, but I think that is only treating part of the problem.
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