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Modulation of chemokine gene expression by Shiga-toxin producing Escherichia coli belonging to various origins and serotypes

机译:产生志贺毒素的大肠杆菌对趋化因子基因表达的调控,该大肠杆菌属于各种来源和血清型

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摘要

Infection with Shiga-toxin producing Escherichia coli (STEC) may result in the development of the haemolytic-uremic syndrome (HUS), the main cause of acute renal failure in children. While O157:H7 STEC are associated with large outbreaks of HUS, it is difficult to predict whether a non-O157:H7 isolate can be pathogenic for humans. The mucosal innate immune response plays a central role in the pathogenesis of HUS; therefore, we compared the induction of IL-8 and CCL20 in human colon epithelial cells infected with strains belonging to different serotypes, isolated from cattle or from HUS patients. No correlation was observed between strain virulence and chemokine gene expression. Rather, the genetic background of the strains seems to determine the chemokine gene expression profile. Investigating the contribution of different bacterial factors in this process, we show that the type III secretion system of O157:H7 bacteria, but not the intimate adhesion, is required to stimulate the cells. In addition, H7, H10, and H21 flagellins are potent inducers of chemokine gene expression when synthesized in large amount.
机译:感染产生志贺毒素的大肠杆菌(STEC)可能导致溶血性尿毒症综合征(HUS)的发展,后者是儿童急性肾衰竭的主要原因。尽管O157:H7 STEC与HUS的大爆发有关,但很难预测非O157:H7分离株是否可能对人类致病。粘膜固有免疫反应在HUS的发病机制中起着核心作用。因此,我们比较了从牛或HUS患者中分离到不同血清型菌株感染的人结肠上皮细胞中IL-8和CCL20的诱导作用。菌株毒力和趋化因子基因表达之间没有相关性。而是,菌株的遗传背景似乎决定了趋化因子基因的表达谱。调查不同细菌因素在此过程中的作用,我们表明刺激细胞需要O157:H7细菌的III型分泌系统,但不是紧密粘附。另外,当大量合成时,H7,H10和H21鞭毛蛋白是趋化因子基因表达的有效诱导物。

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