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.

中文翻译：

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肠道致病性大肠杆菌的毒性，这是一种全球病原体。

肠致病性大肠杆菌（EPEC）仍然是全世界腹泻病的重要原因。对EPEC的研究非常激烈，并为其他大肠杆菌感染以及其他致病细菌提供了良好的毒力模型。尽管现在对毒力机制有了更好的了解，但它们极其复杂，还有很多东西要学习。EPEC的发病机理取决于超微结构病变的形成，在这种病变中，细菌与宿主的顶端肠上皮细胞膜紧密接触。这种损害的形成是EPEC在成束菌毛的辅助下以局部方式粘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发生在宿主细胞内的病变部位，从而导致宿主细胞机制的破坏，并因此导致腹泻。这些是由高度调节的EPEC分泌蛋白的作用产生的，这些蛋白通过III型分泌系统释放，其许多基因位于被称为肠上皮细胞受损部位的致病岛内。在过去的几年中，我们对EPEC毒力的了解急剧增加。因此，本综述旨在提供对EPEC毒力方面的广泛概述和更新。