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肠致病性大肠杆菌的黏附与损伤毒力特性

The attaching and effacing virulence property of enteropathogenic Escherichia coli.

作者信息

Knutton S, Baldwin T, Williams P, Manjarrez-Hernandez A, Aitken A

机构信息

Institute of Child Health, University of Birmingham, U.K.

出版信息

Zentralbl Bakteriol. 1993 Apr;278(2-3):209-17. doi: 10.1016/s0934-8840(11)80838-8.

Abstract

Enteropathogenic Escherichia coli (EPEC) remain an important cause of infant diarrhoea in many parts of the developing world. Essential for virulence is their ability to adhere to the small intestinal mucosa and produce a striking 'attaching and effacing' (AE) lesion characterised by localised destruction of brush border microvilli, intimate attachment of bacteria to the residual apical enterocyte membrane, often in a cuplike pedestal structure, and formation of a dense plaque of actin (and other) cytoskeletal filaments beneath adherent bacteria. Fluorescence actin staining (FAS test) has turned out to be a useful diagnostic test for the AE lesion and also led to the identification of a chromosomal gene, eae, which is necessary but, by itself, not sufficient to produce the AE lesion. The 94 kDa outer membrane protein encoded by eae may be the adhesin which promotes intimate bacterial attachment. The signal transduction pathway which leads to AE lesion formation has yet to be defined although EPEC induced increased levels in intracellular calcium and phosphorylation of specific cell proteins including myosin light chain suggest that EPEC, by binding to a specific host cell receptor, may be promoting a calcium second message which would a) activate the brush border protein villin to cause microvillar breakdown and b) stimulate protein kinase activity to cause the other cytoskeletal rearrangements.

摘要

肠致病性大肠杆菌(EPEC)仍是发展中世界许多地区婴儿腹泻的重要病因。其毒力的关键在于它们能够黏附于小肠黏膜并产生显著的“紧密黏附并抹平”(AE)损伤,其特征为刷状缘微绒毛的局部破坏、细菌与残留顶端肠细胞膜的紧密黏附,细菌常呈杯状基座结构,以及在黏附细菌下方形成密集的肌动蛋白(及其他)细胞骨架丝斑块。荧光肌动蛋白染色(FAS试验)已成为诊断AE损伤的有用检测方法,还促成了一个染色体基因eae的鉴定,该基因是产生AE损伤所必需的,但仅靠自身并不足以导致这种损伤。由eae编码的94 kDa外膜蛋白可能是促进细菌紧密黏附的黏附素。尽管EPEC可导致细胞内钙水平升高以及包括肌球蛋白轻链在内的特定细胞蛋白磷酸化,提示EPEC通过与特定宿主细胞受体结合,可能促进一种钙第二信使,该信使会:a)激活刷状缘蛋白绒毛蛋白导致微绒毛破坏;b)刺激蛋白激酶活性导致其他细胞骨架重排,但导致AE损伤形成的信号转导途径尚未明确。

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