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新型质粒编码 Clp ATP 酶 ClpK 介导的耐热性可能是肺炎克雷伯菌医院内定植的新机制。

Heat resistance mediated by a new plasmid encoded Clp ATPase, ClpK, as a possible novel mechanism for nosocomial persistence of Klebsiella pneumoniae.

机构信息

Department of Microbiological Surveillance and Research, Statens Serum Institut, Copenhagen, Denmark.

出版信息

PLoS One. 2010 Nov 9;5(11):e15467. doi: 10.1371/journal.pone.0015467.

Abstract

Klebsiella pneumoniae is an important opportunistic pathogen and a frequent cause of nosocomial infections. We have characterized a K. pneumoniae strain responsible for a series of critical infections in an intensive care unit over a two-year period. The strain was found to be remarkably thermotolerant providing a conceivable explanation of its persistence in the hospital environment. This marked phenotype is mediated by a novel type of Clp ATPase, designated ClpK. The clpK gene is encoded by a conjugative plasmid and we find that the clpK gene alone renders an otherwise sensitive E. coli strain resistant to lethal heat shock. Furthermore, one third of a collection of nosocomial K. pneumoniae isolates carry clpK and exhibit a heat resistant phenotype. The discovery of ClpK as a plasmid encoded factor and its profound impact on thermal stress survival sheds new light on the biological relevance of Clp ATPases in acquired environmental fitness and highlights the challenges of mobile genetic elements in fighting nosocomial infections.

摘要

肺炎克雷伯菌是一种重要的机会致病菌,也是医院感染的常见病因。我们对在重症监护病房(ICU)中引起一系列严重感染的肺炎克雷伯菌进行了研究,该菌在长达两年的时间内一直存在于医院环境中,表现出很强的耐热性,这为其在医院环境中的持续存在提供了一个合理的解释。这种显著的表型是由一种新型的 Clp ATPase 介导的,被命名为 ClpK。clpK 基因由一个可接合的质粒编码,我们发现 clpK 基因本身就能使原本敏感的大肠杆菌菌株对致死性热激产生抗性。此外,我们收集的三分之一医院获得性肺炎克雷伯菌分离株携带 clpK 基因,表现出耐热表型。ClpK 作为一种质粒编码因子的发现及其对热应激存活的深远影响,揭示了 Clp ATPases 在获得性环境适应性方面的生物学相关性,并强调了移动遗传元件在防治医院感染方面所面临的挑战。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b4c/2976762/b0a0cbc9701a/pone.0015467.g001.jpg

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