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首页> 外文期刊>Infection and immunity >Contribution of the Twin Arginine Translocation System to the Virulence of Enterohemorrhagic Escherichia coli O157:H7
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Contribution of the Twin Arginine Translocation System to the Virulence of Enterohemorrhagic Escherichia coli O157:H7

机译:双精氨酸转运系统对肠出血性大肠杆菌O157:H7的毒力的贡献

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Shiga toxin-producing Escherichia coli O157:H7 is a major food-borne infectious pathogen. In order to analyze the contribution of the twin arginine translocation (TAT) system to the virulence of E. coli O157:H7, we deleted the tatABC genes of the O157:H7 EDL933 reference strain. The mutant displayed attenuated toxicity on Vero cells and completely lost motility on soft agar plates. Further analyses revealed that the ΔtatABC mutation impaired the secretion of the Shiga toxin 1 (Stx1) and abolished the synthesis of H7 flagellin, which are two major known virulence factors of enterohemorrhagic E. coli O157:H7. Expression of the EDL933 stxAB1 genes in E. coli K-12 conferred verotoxicity on this nonpathogenic strain. Remarkably, cytotoxicity assay and immunoblot analysis showed, for the first time, an accumulation of the holotoxin complex in the periplasm of the wild-type strain and that a much smaller amount of StxA1 and reduced verotoxicity were detected in the ΔtatC mutant cells. Together, these results establish that the TAT system of E. coli O157:H7 is an important virulence determinant of this enterohemorrhagic pathogen.
机译:产生志贺毒素的大肠杆菌 O157:H7是主要的食源性传染病原体。为了分析双精氨酸易位(TAT)系统对 E毒力的贡献。大肠杆菌 O157:H7,我们删除了O157:H7 EDL933参考菌株的 tatABC 基因。该突变体在Vero细胞上显示出减弱的毒性,在软琼脂板上完全丧失了运动能力。进一步的分析表明,Δ tatABC 突变损害了志贺毒素1(Stx1)的分泌,并取消了H7鞭毛蛋白的合成,而鞭毛蛋白是肠出血性 E的两个主要已知毒力因子。大肠杆菌O157:H7。 EDL933 stxAB 1 基因在 E中的表达。大肠杆菌K-12对这种非致病性菌株具有病毒毒性。值得注意的是,细胞毒性测定和免疫印迹分析首次显示了野生型菌株周质中的全毒素复合物的积累,并且检测到的StxA 1 量更小并且降低了垂直毒性在Δ tatC 突变细胞中。这些结果共同证明了 E的TAT系统。 O157:H7大肠杆菌是这种肠出血性病原体的重要毒力决定因素。

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