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The cytochrome bd-I respiratory oxidase augments survival of multidrug-resistant Escherichia coli during infection

机译:细胞色素bd-I呼吸氧化酶在感染过程中提高了耐多药大肠杆菌的存活率

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摘要

Nitric oxide (NO) is a toxic free radical produced by neutrophils and macrophages in response to infection. Uropathogenic Escherichia coli (UPEC) induces a variety of defence mechanisms in response to NO, including direct NO detoxification (Hmp, NorVW, NrfA), iron-sulphur cluster repair (YtfE), and the expression of the NO-tolerant cytochrome bd-I respiratory oxidase (CydAB). The current study quantifies the relative contribution of these systems to UPEC growth and survival during infection. Loss of the flavohemoglobin Hmp and cytochrome bd-I elicit the greatest sensitivity to NO-mediated growth inhibition, whereas all but the periplasmic nitrite reductase NrfA provide protection against neutrophil killing and promote survival within activated macrophages. Intriguingly, the cytochrome bd-I respiratory oxidase was the only system that augmented UPEC survival in a mouse model after 2 days, suggesting that maintaining aerobic respiration under conditions of nitrosative stress is a key factor for host colonisation. These findings suggest that while UPEC have acquired a host of specialized mechanisms to evade nitrosative stresses, the cytochrome bd-I respiratory oxidase is the main contributor to NO tolerance and host colonisation under microaerobic conditions. This respiratory complex is therefore of major importance for the accumulation of high bacterial loads during infection of the urinary tract.
机译:一氧化氮(NO)是嗜中性粒细胞和巨噬细胞响应感染而产生的有毒自由基。致病性大肠杆菌(UPEC)对NO诱导多种防御机制,包括直接NO排毒(Hmp,NorVW,NrfA),铁硫簇修复(YtfE)以及耐NO细胞色素bd-I的表达呼吸氧化酶(CydAB)。当前的研究量化了这些系统在感染期间对UPEC生长和存活的相对贡献。黄素血红蛋白Hmp和细胞色素bd-I的丢失引起对NO介导的生长抑制的最大敏感性,而除周质亚硝酸还原酶NrfA以外的所有蛋白均提供抗中性粒细胞杀伤的保护并促进活化巨噬细胞的存活。有趣的是,细胞色素bd-I呼吸氧化酶是2天后唯一增加UPEC存活率的系统,表明在亚硝化胁迫条件下维持有氧呼吸是宿主定殖的关键因素。这些发现表明,尽管UPEC已获得许多逃避亚硝化胁迫的专门机制,但细胞色素bd-I呼吸氧化酶是NO耐受性和在微有氧条件下宿主定殖的主要因素。因此,这种呼吸复合体对于尿路感染期间高细菌负荷的积累至关重要。

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