期刊
INFLAMMATORY BOWEL DISEASES
卷 13, 期 9, 页码 1153-1164出版社
OXFORD UNIV PRESS INC
DOI: 10.1002/ibd.20174
关键词
inflammatory bowel diseases; intestinal epithelial cells; nuclear transcription factor kappa B (NF-kappa B); host-derived anti-inflammatory signals; endoplasmic reticulum stress; glucose regulated protein (Grp)-78; interleukin 10; commensal bacteria
The genetic predisposition to deregulated mucosal immune responses and the concurrent prevalence of certain environmental triggers in developed countries are strong etiologic factors for the development of inflammatory bowel diseases in human subjects, including Crohn's disease and ulcerative colitis. Numerous clinical and experimental studies have shown that the intestinal microbes are critical for the initiation and progression of chronic intestinal inflammation. Activation of pattern recognition receptor signaling via members of the Toll-like receptor (TLR) and the nucleotide-binding oligomerization domain (NOD)-like families initiates inflammatory defense mechanisms that are required to alert and protect the host. Key inflammatory mechanisms such as nuclear transcription factor kappa B (NF-kappa B) activation and endoplasmic reticuturn stress responses are controlled by a complex network of pathways that includes intrinsic feedback effectors and is targeted by immunosuppressive cytokines such as interleukin 10 (IL-10) and transforming growth factor (TGF-beta)-p. In the absence or after functional loss of these anti i nfl ammatory feedback signals, physiological defense mechanisms may turn into pathological responses. The data discussed in the present review suggest that disturbances in the homeostasis between bacteria- and host-derived signals at the epithelial cell level lead to a break in the intestinal barrier function and to the development of mucosal immune disorders in genetically susceptible hosts.
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