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首页> 外文期刊>Infection and immunity >Requirement of the Shigella flexneri Virulence Plasmid in the Ability To Induce Trafficking of Neutrophils across Polarized Monolayers of the Intestinal Epithelium
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Requirement of the Shigella flexneri Virulence Plasmid in the Ability To Induce Trafficking of Neutrophils across Polarized Monolayers of the Intestinal Epithelium

机译：弗氏志贺氏菌毒力质粒在诱导嗜中性粒细胞跨过肠道上皮极化单层的运输中的要求。

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Attachment of an array of enteric pathogens to epithelial surfaces is accompanied by recruitment of polymorphonuclear leukocytes (PMN) across the intestinal epithelium. In this report, we examine howShigella-intestinal epithelium interactions evoke the mucosal inflammatory response. We modeled these interactions in vitro by using polarized monolayers of the human intestinal epithelial cell line, T84, isolated human PMNs, and Shigella flexneri. We show that Shigella attachment to T84-cell basolateral membranes was a necessary component in the signaling cascade for induction of basolateral-to-apical directed transepithelial PMN migration, the direction of PMN transepithelial migration in vivo. In contrast, attachment of Shigella to the T84-cell apical membrane failed to stimulate a directed PMN transepithelial migration response. Importantly, the ability of Shigella to induce PMN migration across epithelial monolayers was dependent on the presence of the 220-kb virulence plasmid. Moreover, examination ofShigella genes necessary to signal subepithelial neutrophils established the requirement of a functional type III secretion system. Our results indicate that the ability ofShigella to elicit transepithelial signaling to neutrophils from the basolateral membrane of epithelial cells represents a mechanism involved in Shigella-elicited enteritis in humans.
机译：一系列肠道病原体附着在上皮表面会伴随着多形核白细胞（PMN）在肠道上皮的募集。在本报告中，我们研究了志贺氏菌-肠上皮相互作用如何引起粘膜炎症反应。我们使用人类肠道上皮细胞系，T84，分离的人类PMN和弗氏志贺氏菌的极化单层体外模拟了这些相互作用。我们显示志贺氏菌对T84细胞基底外侧膜的附着是信号级联反应中诱导基底外侧向顶端定向上皮PMN迁移（体内PMN跨上皮迁移方向）的必要组成部分。相比之下，志贺氏菌附着于T84细胞顶膜不能刺激定向的PMN跨上皮迁移反应。重要的是，志贺氏菌诱导PMN跨上皮单层迁移的能力取决于220 kb毒力质粒的存在。此外，对发信号给上皮下嗜中性粒细胞的<志>志贺氏菌基因的检查确立了功能性III型分泌系统的要求。我们的结果表明，志贺氏菌从上皮细胞的基底外侧膜引起嗜中性白细胞经上皮信号转导的能力代表了人类志贺氏菌引起的肠炎的一种机制。

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