Ulcerative colitis and Crohn's disease occur in regions of the intestine colonized by the highest concentrations of normal flora bacteria and resemble certain chronic bacterial, viral or parasitic infections. However, the role of endogenous and pathogenic bacteria in the induction and perpetuation of chronic idiopathic intestinal inflammation remains controversial. No convincing evidence incriminates a single bacterial, mycobacterial or viral agent as the cause of a high percentage of cases of idiopathic inflammatory bowel disease (IBD). Subtle alterations of luminal microbial flora are nearly impossible to detect, but concentrations of certain anaerobic bacteria, including Bacteroides vulgatus, are increased in active Crohn's disease and correlate with disease activity. Recent investigations suggest mechanisms which bacteria may induce an autoimmune response through molecular mimicry or alterations in host antigens or immunoregulation. Intestinal bacteria contain formylated peptides and cell wall polymers ( endotoxin and peptidoglycan-polysaccharide complexes) which have potent and well characterized inflammatory and immunoregulatory properties and can produce acute and chronic intestinal and systemic inflammation in experimental animals. These proinflammatory molecules are probably absorbed more readily in IBO due ro increased mucosa! permeability during active and perhaps quiescent phases of disease. While the primary mechanisms of intestinal injury remain unknown, it is likely that commensal bacteria and their products amplify and perpetuate the inflammatory response of IBO and may be responsible for extraintestinal manifestations in addition to the frequent septic complications of these diseases.
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