The possible role of anaerobes in inflammatory bowel disease ( ulcerative colitis and Crohn's disease)

The distal ileum and colon harbors very high concentrations of bacteria. These may include potential pathogens that could initiate inflammatory bowel disease (IBD). Increased underlying genetic predisposition due to genetic mucosal or immune defect may enhance IBD in some individuals. As study by sutton et al provided support for this hypothesis in finding of an immune response directed against a particular bacterial DNA segment (I2) in affected mucosa from 54 % of patients with Crohn's disease compared to 4 to 10 % of normal individuals. However, no specific organism has been shown to have a consistent relationship to IBD.

Because of the high number of anaerobic bacteria within the intestinal flora, any disturbance of the intestinal epithelium could generate an inflammatory response. This can be due to the effects of microbial products that effect  the underlying epithelium, or from defects in the epithelium which permits bacterial and food antigens to stimulate the mucosal immune system. Studies in genetically engineered mice support the importance of an intact epithelium as an altered gut epithelium lead to the development of spontaneous colitis. Genetic studies have described susceptibility loci that regulate innate responses to the microbial flora and provide support for the role of microbes in the pathogenesis of IBD.

 The ability of the microbial flora to induce disease has been demonstrated in murine models of IBD. A genetically engineered mice that was deficient in cytokines IL-2 and IL-10 or rats containing the HLA-B27 transgene develop inflammatory bowel disease in the presence of a normal microflora but not in germ-free conditions. Mow et al found that immunoreactivity to microbial antigens correlates with complications of small bowel Crohn's disease in humans.