作者: R. Balfour Sartor
DOI: 10.1128/9781555817848.CH13
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摘要: This chapter outlines evidence supporting the hypothesis that chronic immune-mediated intestinal inflammation in genetically susceptible hosts is a consequence of overly aggressive cell-mediated immune responses to subset commensal luminal bacteria. The most compelling normal bacteria induce colitis fact at least 11 separate models induced or spontaneous inflammation, no disease occurs absence (germ free sterile state). Recent results several independent gnotobiotic demonstrate enteric bacterial species differ their capacity inflammation. Chronic mediated by T lymphocytes, based on experimental T-cell-deficient hosts, induction transfer CD4 + and prevention reversal blockade products TH1 cytokines. A key factor loss tolerance antigens hosts. Many studies discussed support an cell response complex resident population Results animal indicate manipulation microflora antibiotics, probiotics, prebiotics can treat established prevent recurrent These physiologic manipulations may have additive perhaps synergistic activities with more widely used immunosuppressive therapies emerging growth treatments.