Hofman P
Equipe INSERM 02-15, IFR 50, Faculté de Médecine, Avenue de Valombrose, 06107 Nice, Cédex 02, France.
Cell Mol Biol (Noisy-le-grand). 2003 Feb;49(1):65-75.
Communication between bacteria and the gastrointestinal tight junctions (TJs) and zonula adherens is examined. Bacteial-epithelial TJs "crosstalk" can be mediated by many virulence factors, mainly secreted toxins, or can be induced by direct contact of the pathogen with epithelial membrane. Moreover, there are several mechanisms by which bacteria may act on gastrointestinal TJs. First, bacteria can act indirectely at the TJs level by inducing cell transepithelial migration. More particularly, neutrophil or dendritic cells can cross the epithelium by a paracellular pathway. Secondly, bacteria and/or toxins can trigger actin cytoskeleton reorganization (depolymerization or hyperpolymerization). Thirdly, some enteric pathogens are susceptible to act on TJs by activation of cellular signal transduction. Finally, cleavage or modification of TJs proteins can be used by bacteria. New therapeutic strategies may result from a deeper knowledge of the cellular and molecular processes induced by bacteria at the TJ level. Moreover, studies of action of the different bacterial virulence factors on the molecules comprising the TJs and zonula adherens allow us an interesting approach on our understanding of TJ complex regulation.
研究了细菌与胃肠道紧密连接(TJ)和黏着连接之间的相互作用。细菌与上皮细胞紧密连接的“串扰”可由多种毒力因子介导,主要是分泌毒素,也可由病原体与上皮细胞膜的直接接触诱导。此外,细菌作用于胃肠道紧密连接有多种机制。首先,细菌可通过诱导细胞跨上皮迁移间接作用于紧密连接水平。更具体地说,中性粒细胞或树突状细胞可通过细胞旁途径穿过上皮。其次,细菌和/或毒素可触发肌动蛋白细胞骨架重组(解聚或过度聚合)。第三,一些肠道病原体可通过激活细胞信号转导作用于紧密连接。最后,细菌可对紧密连接蛋白进行切割或修饰。对细菌在紧密连接水平诱导的细胞和分子过程有更深入的了解可能会产生新的治疗策略。此外,研究不同细菌毒力因子对构成紧密连接和黏着连接的分子的作用,有助于我们有趣地理解紧密连接复合体的调节。