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II 型分泌系统及其普遍存在的脂蛋白底物 SslE,是肠致病性大肠杆菌生物膜形成和毒力所必需的。

The type II secretion system and its ubiquitous lipoprotein substrate, SslE, are required for biofilm formation and virulence of enteropathogenic Escherichia coli.

机构信息

Department of Microbiology and Immunology, The University of Melbourne, Melbourne, Australia.

出版信息

Infect Immun. 2012 Jun;80(6):2042-52. doi: 10.1128/IAI.06160-11. Epub 2012 Mar 26.

Abstract

Enteropathogenic Escherichia coli (EPEC) is a major cause of diarrhea in infants in developing countries. We have identified a functional type II secretion system (T2SS) in EPEC that is homologous to the pathway responsible for the secretion of heat-labile enterotoxin by enterotoxigenic E. coli. The wild-type EPEC T2SS was able to secrete a heat-labile enterotoxin reporter, but an isogenic T2SS mutant could not. We showed that the major substrate of the T2SS in EPEC is SslE, an outer membrane lipoprotein (formerly known as YghJ), and that a functional T2SS is essential for biofilm formation by EPEC. T2SS and SslE mutants were arrested at the microcolony stage of biofilm formation, suggesting that the T2SS is involved in the development of mature biofilms and that SslE is a dominant effector of biofilm development. Moreover, the T2SS was required for virulence, as infection of rabbits with a rabbit-specific EPEC strain carrying a mutation in either the T2SS or SslE resulted in significantly reduced intestinal colonization and milder disease.

摘要

肠致病性大肠杆菌(EPEC)是发展中国家婴儿腹泻的主要病因。我们在 EPEC 中发现了一种功能性 II 型分泌系统(T2SS),与肠产毒性大肠杆菌中负责分泌不耐热肠毒素的途径同源。野生型 EPEC T2SS 能够分泌不耐热肠毒素报告基因,但同基因 T2SS 突变体则不能。我们表明,EPEC T2SS 的主要底物是 SslE,一种外膜脂蛋白(以前称为 YghJ),并且功能性 T2SS 对于 EPEC 生物膜形成是必需的。T2SS 和 SslE 突变体在生物膜形成的微菌落阶段被阻断,表明 T2SS 参与成熟生物膜的发育,并且 SslE 是生物膜发育的主要效应因子。此外,T2SS 对于毒力是必需的,因为用携带 T2SS 或 SslE 突变的兔特异性 EPEC 菌株感染兔子会导致肠道定植明显减少和疾病减轻。

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