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肠致病性大肠杆菌与宿主上皮细胞的相互作用。

Interaction of enteropathogenic Escherichia coli with host epithelial cells.

作者信息

Nisan I, Wolff C, Hanski E, Rosenshine I

机构信息

Department of Molecular Genetics and Biotechnology, Hebrew University, Faculty of Medicine, Jerusalem, Israel.

出版信息

Folia Microbiol (Praha). 1998;43(3):247-52. doi: 10.1007/BF02818609.

Abstract

Enteropathogenic Escherichia coli (EPEC) causes severe diarrhea in young children. Upon infection, EPEC induces the assembly of highly organized pedestal-like actin structures in host epithelial cells. All the EPEC genes that are involved in inducing formation of actin pedestals are located in a unique 35 kbp chromosomal pathogenicity island, termed LEE. These genes include the sep genes that encode components of type III protein secretion system, and genes that encode proteins secreted by this system, the esp genes. This protein secretion system is activated upon contact with the host cell, resulting in increased secretion of Esp proteins. Some of these Esp proteins from the translocation apparatus while others are translocated into the cytoplasm of the host cell. Concerted activity of the LEE genes including the eae, esp and the sep genes is needed to trigger signal transduction in the host cell which results in formation of an actin pedestal.

摘要

肠致病性大肠杆菌(EPEC)可导致幼儿严重腹泻。感染后,EPEC会诱导宿主上皮细胞中形成高度有序的基座样肌动蛋白结构。所有参与诱导肌动蛋白基座形成的EPEC基因都位于一个独特的35千碱基对的染色体致病岛,称为LEE。这些基因包括编码III型蛋白分泌系统组分的sep基因,以及编码由该系统分泌的蛋白的基因,即esp基因。该蛋白分泌系统在与宿主细胞接触时被激活,导致Esp蛋白分泌增加。这些Esp蛋白中的一些来自转运装置,而其他的则被转运到宿主细胞的细胞质中。需要包括eae、esp和sep基因在内的LEE基因协同作用来触发宿主细胞中的信号转导,从而导致肌动蛋白基座的形成。

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