Michael Smith Laboratories, University of British Columbia, Vancouver, BC, Canada.
Michael Smith Laboratories, University of British Columbia, Vancouver, BC, Canada; Department of Microbiology and Immunology, University of British Columbia, Vancouver, BC, Canada; Department of Biochemistry and Molecular Biology, University of British Columbia, Vancouver, BC, Canada.
Curr Opin Microbiol. 2020 Apr;54:67-76. doi: 10.1016/j.mib.2019.12.001. Epub 2020 Feb 12.
Enteropathogenic Escherichia coli (EPEC) is an important cause of infant diarrhea and mortality worldwide. The locus of enterocyte effacement (LEE) pathogenicity island in the EPEC genome encodes a type 3 secretion system (T3SS). This nanomachine directly injects a sophisticated arsenal of effectors into host cells, which is critical for EPEC pathogenesis. To colonize the gut mucosa, EPEC alters its gene expression in response to host environmental signals. Regulation of the LEE has been studied extensively, revealing key mechanisms of transcriptional regulation, and more recently at the posttranscriptional and posttranslational levels. Moreover, the T3SS assembly and secretion is a highly coordinated process that ensures hierarchical delivery of effectors upon cell contact. EPEC effectors and virulence factors not only manipulate host cellular processes, but also modulate effector translocation by controlling T3SS formation. In this review, we focus on the regulation of EPEC virulence genes and modulation of effector secretion and translocation.
肠致病性大肠杆菌（EPEC）是全球范围内导致婴儿腹泻和死亡的重要原因。EPEC 基因组中的肠上皮细胞消失（LEE）致病性岛编码一种 III 型分泌系统（T3SS）。这种纳米机器直接将一系列复杂的效应器注入宿主细胞，这对 EPEC 的发病机制至关重要。为了在肠道黏膜上定植，EPEC 会根据宿主环境信号改变其基因表达。LEE 的调控已经得到了广泛的研究，揭示了转录调控的关键机制，最近还研究了转录后和翻译后水平的调控。此外，T3SS 的组装和分泌是一个高度协调的过程，确保了在细胞接触时按层次递效器。EPEC 的效应器和毒力因子不仅操纵宿主细胞的过程，还通过控制 T3SS 的形成来调节效应器的易位。在这篇综述中，我们重点关注 EPEC 毒力基因的调控以及效应器分泌和易位的调节。
