Dysbiosis, or altered intestinal bacterial flora, is thought by many to play an important role in the pathogenesis of IBD. NOD2 is involved in the recognition of specific bacterial peptides and subsequent activation of an immune response. Studies with different mouse models of IBD have shown that certain bacterial strains are protective while others are not. For example, in IL-2 deficient mice, colitis was induced with an Escherichia coli mpk strain, but not with Bacteroides vulgatus. If both of these were administered together, colitis was not observed. This indicates that B vulgatus may serve a protective role, at least in this model.
In an IL-10 deficient mouse model, Lactobacillus reuteri was shown to positively affect inflammation, and in some cases, even prevent the development of colitis. Increased levels of IL-10 down-regulate the production of interferon gamma, known to play a key role in granuloma formation. (Granulomas are identifying pathologic features of Crohn's disease.) On the other hand, Enterococcus faecalis has been shown to precipitate colitis in this same mouse model.
Schistosoma mansoni eggs down-regulate Th1-mediated inflammation in a trinitrobenzene sulphonic acid model of colitis. Increased IL-4, increased IL-10 mRNA and decreased interferon gamma levels were noted.
In ulcerative colitis, a preliminary trial showed Saccharomyces boulardii to be effective in treatment.
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Cite this: Dietary Factors in the Modulation of Inflammatory Bowel Disease Activity - Medscape - Mar 27, 2007.