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直觉:肠致病性大肠杆菌(EPEC)与宿主的相互作用

Gut feelings: enteropathogenic E. coli (EPEC) interactions with the host.

作者信息

Goosney D L, Gruenheid S, Finlay B B

机构信息

The Biotechnology Laboratory and the Department of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada.

出版信息

Annu Rev Cell Dev Biol. 2000;16:173-89. doi: 10.1146/annurev.cellbio.16.1.173.

Abstract

Enteropathogenic Escherichia coli (EPEC) is a gram-negative bacterial pathogen that adheres to human intestinal epithelial cells, resulting in watery, persistent diarrhea. It subverts the host cell cytoskeleton, causing a rearrangement of cytoskeletal components into a characteristic pedestal structure underneath adherent bacteria. In contrast to other intracellular pathogens that affect the actin cytoskeleton from inside the host cytoplasm, EPEC remains extracellular and transmits signals through the host cell plasma membrane via direct injection of virulence factors by a "molecular syringe," the bacterial type III secretion system. One injected factor is Tir, which functions as the plasma membrane receptor for EPEC adherence. Tir directly links extracellular EPEC through the epithelial membrane and firmly anchors it to the host cell actin cytoskeleton, thereby initiating pedestal formation. In addition to stimulating actin nucleation and polymerization in the host cell, EPEC activates several other signaling pathways that lead to tight junction disruption, inhibition of phagocytosis, altered ion secretion, and immune responses. This review summarizes recent developments in our understanding of EPEC pathogenesis and discusses similarities and differences between EPEC pedestals, focal contacts, and Listeria monocytogenes actin tails.

摘要

肠致病性大肠杆菌(EPEC)是一种革兰氏阴性细菌病原体,它粘附于人类肠道上皮细胞,导致水样持续性腹泻。它会破坏宿主细胞的细胞骨架,使细胞骨架成分重新排列,在粘附细菌下方形成特征性的基座结构。与其他从宿主细胞质内部影响肌动蛋白细胞骨架的细胞内病原体不同,EPEC 仍位于细胞外,并通过“分子注射器”即细菌 III 型分泌系统直接注射毒力因子,通过宿主细胞质膜传递信号。其中一个注射因子是 Tir,它作为 EPEC 粘附的质膜受体。Tir 通过上皮膜直接连接细胞外的 EPEC,并将其牢固地锚定在宿主细胞肌动蛋白细胞骨架上,从而启动基座形成。除了刺激宿主细胞中的肌动蛋白成核和聚合外,EPEC 还激活其他几种信号通路,导致紧密连接破坏、吞噬作用抑制、离子分泌改变和免疫反应。本综述总结了我们对 EPEC 发病机制理解的最新进展,并讨论了 EPEC 基座、粘着斑和单核细胞增生李斯特菌肌动蛋白尾之间的异同。

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