Regulation of intestinal epithelial permeability by tight junctions

被引:1486
作者
Suzuki, Takuya [1 ]
机构
[1] Hiroshima Univ, Dept Biofunct Sci & Technol, Grad Sch Biosphere Sci, Higashihiroshima 7398528, Japan
基金
日本学术振兴会;
关键词
Tight junction; Intestinal epithelium; Cytokine; Pathogen; Nutrient; NECROSIS-FACTOR-ALPHA; CLOSTRIDIUM-PERFRINGENS ENTEROTOXIN; INFLAMMATORY-BOWEL-DISEASE; CACO-2 CELL MONOLAYERS; ENTEROPATHOGENIC ESCHERICHIA-COLI; CHAIN FATTY-ACIDS; PROTEIN-KINASE-C; EPIDERMAL-GROWTH-FACTOR; KAPPA-B ACTIVATION; ACETALDEHYDE-INDUCED INCREASE;
D O I
10.1007/s00018-012-1070-x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
The gastrointestinal epithelium forms the boundary between the body and external environment. It effectively provides a selective permeable barrier that limits the permeation of luminal noxious molecules, such as pathogens, toxins, and antigens, while allowing the appropriate absorption of nutrients and water. This selective permeable barrier is achieved by intercellular tight junction (TJ) structures, which regulate paracellular permeability. Disruption of the intestinal TJ barrier, followed by permeation of luminal noxious molecules, induces a perturbation of the mucosal immune system and inflammation, and can act as a trigger for the development of intestinal and systemic diseases. In this context, much effort has been taken to understand the roles of extracellular factors, including cytokines, pathogens, and food factors, for the regulation of the intestinal TJ barrier. Here, I discuss the regulation of the intestinal TJ barrier together with its implications for the pathogenesis of diseases.
引用
收藏
页码:631 / 659
页数:29
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