Clarke S C, Haigh R D, Freestone P P E, Williams P H
Scottish Meningococcus and Pneumococcus Reference Laboratory, Glasgow University, Glasgow, United Kingdom.
Clin Microbiol Rev. 2003 Jul;16(3):365-78. doi: 10.1128/CMR.16.3.365-378.2003.
Enteropathogenic Escherichia coli (EPEC) remains an important cause of diarrheal disease worldwide. Research into EPEC is intense and provides a good virulence model of other E. coli infections as well as other pathogenic bacteria. Although the virulence mechanisms are now better understood, they are extremely complex and much remains to be learnt. The pathogenesis of EPEC depends on the formation of an ultrastructural lesion in which the bacteria make intimate contact with the host apical enterocyte membrane. The formation of this lesion is a consequence of the ability of EPEC to adhere in a localized manner to the host cell, aided by bundle-forming pili. Tyrosine phosphorylation and signal transduction events occur within the host cell at the lesion site, leading to a disruption of the host cell mechanisms and, consequently, to diarrhea. These result from the action of highly regulated EPEC secreted proteins which are released via a type III secretion system, many genes of which are located within a pathogenicity island known as the locus of enterocyte effacement. Over the last few years, dramatic increases in our knowledge of EPEC virulence have taken place. This review therefore aims to provide a broad overview of and update to the virulence aspects of EPEC.
肠致病性大肠杆菌（EPEC）仍是全球腹泻病的一个重要病因。对EPEC的研究十分深入，它为其他大肠杆菌感染以及其他病原菌提供了一个良好的毒力模型。尽管目前对其毒力机制有了更好的理解，但它们极其复杂，仍有许多有待了解之处。EPEC的发病机制取决于一种超微结构损伤的形成，在此过程中细菌与宿主顶端肠细胞膜紧密接触。这种损伤的形成是EPEC借助束状菌毛以局部方式黏附于宿主细胞的能力的结果。酪氨酸磷酸化和信号转导事件在宿主细胞内的损伤部位发生，导致宿主细胞机制紊乱，进而引发腹泻。这些是由高度调控的EPEC分泌蛋白的作用引起的，这些蛋白通过Ⅲ型分泌系统释放，其中许多基因位于一个称为肠细胞损伤位点的致病岛内。在过去几年里，我们对EPEC毒力的认识有了显著增加。因此，本综述旨在对EPEC的毒力方面提供一个广泛的概述和更新。
