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首页> 外文期刊>Infection and immunity >Mutations That Impact the Enteropathogenic Escherichia coli Cpx Envelope Stress Response Attenuate Virulence in Galleria mellonella
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Mutations That Impact the Enteropathogenic Escherichia coli Cpx Envelope Stress Response Attenuate Virulence in Galleria mellonella

机译：影响肠道致病性大肠杆菌Cpx信封应力反应的突变减弱了马勒菌廊中的毒力。

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In this paper, we show that the larvae of the greater wax moth, Galleria mellonella, can be used as a model to study enteropathogenic Escherichia coli (EPEC) virulence. G. mellonella larvae are killed after infection with EPEC type strain E2348/69 but not by an attenuated derivative that expresses diminished levels of the major virulence determinants or by a mutant specifically defective in type III secretion (T3S). Infecting EPEC inhabit the larval hemocoel only briefly and then become localized to melanized capsules, where they remain extracellular. Previously, it was shown that mutations affecting the Cpx envelope stress response lead to diminished expression of the bundle-forming pilus (BFP) and the type III secretion system (T3SS). We demonstrate that mutations that activate the Cpx pathway have a dramatic effect on the ability of the bacterium to establish a lethal infection, and this is correlated with an inability to grow in vivo. Infection with all E. coli strains led to increased expression of the antimicrobial peptides (AMPs) gloverin and cecropin, although strain- and AMP-specific differences were observed, suggesting that the G. mellonella host perceives attenuated strains and Cpx mutants in unique manners. Overall, this study shows that G. mellonella is an economical, alternative infection model for the preliminary study of EPEC host-pathogen interactions, and that induction of the Cpx envelope stress response leads to defects in virulence.
机译：在本文中，我们表明，较大的蜡蛾幼虫，Galleria mellonella，可以用作研究肠道致病性大肠杆菌（EPEC）毒力的模型。用EPEC型菌株E2348 / 69感染后，可杀死melonella mel。幼虫，但不能通过表达主要毒力决定簇水平降低的减毒衍生物或通过III型分泌（T3S）特异的突变体杀死。感染EPEC仅短暂停留在幼虫的血小管中，然后定位于黑色素化的囊中，在那里它们仍留在细胞外。以前，已表明影响Cpx包膜应力反应的突变导致成束菌毛（BFP）和III型分泌系统（T3SS）的表达减少。我们证明，激活Cpx途径的突变对细菌建立致命感染的能力具有戏剧性影响，并且这与无法在体内生长有关。尽管观察到菌株和AMP的特异性差异，但所有大肠杆菌菌株的感染均导致抗菌肽（AMPs）手套蛋白和头孢克林的表达增加，这表明G.mellonella宿主以独特的方式感知到减毒的菌株和Cpx突变体。总体而言，这项研究表明，对于G. mellonella是一种经济，替代的感染模型，可以用于EPEC宿主-病原体相互作用的初步研究，并且Cpx包膜应激反应的诱导会导致毒力缺陷。

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