作者: R. Balfour Sartor
DOI: 10.1016/B978-012394330-9/50025-9
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摘要: Publisher Summary Although ulcerative colitis and Crohn's disease appear to be the result of an unrestrained inflammatory response, antigen(s) which initiate perpetuate these chronic, relapsing disorders remain uncertain. Clinicians have a longstanding belief that normal enteric microbial flora were somehow involved in pathogenesis diseases because inflammation occurs distal ileum colon, antibiotics bowel rest benefit patients with disease, (IBD) increased immune responses ubiquitous luminal bacteria. Recent investigations using older induced models intestinal new genetically engineered rodent develop spontaneous enterocolitis provide compelling evidence support hypothesis bacteria their products can induce chronic systemic susceptible hosts. This is rational, given high concentrations predominantly anaerobic bacterial components colon. Mucosal enhances mucosal uptake transport promotes secondary invasion ulcers fistulae by These phlogistic constituents activate phagocytic cells lymphocytes secrete proinflammatory cytokines soluble mediators stimulate specific process. chapter summarizes generated animal supports this hypothesis.