| Summary: | 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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