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Molecular mechanisms and clinical implications of bacterial persistence
Drug Resistance Updates ( IF 24.3 ) Pub Date : 2016-10-15 , DOI: 10.1016/j.drup.2016.10.002
Joran Elie Michiels , Bram Van den Bergh , Natalie Verstraeten , Jan Michiels

Any bacterial population harbors a small number of phenotypic variants that survive exposure to high concentrations of antibiotic. Importantly, these so-called ‘persister cells’ compromise successful antibiotic therapy of bacterial infections and are thought to contribute to the development of antibiotic resistance. Intriguingly, drug-tolerant persisters have also been identified as a factor underlying failure of chemotherapy in tumor cell populations. Recent studies have begun to unravel the complex molecular mechanisms underlying persister formation and revolve around stress responses and toxin–antitoxin modules. Additionally, in vitro evolution experiments are revealing insights into the evolutionary and adaptive aspects of this phenotype. Furthermore, ever-improving experimental techniques are stimulating efforts to investigate persisters in their natural, infection-associated, in vivo environment. This review summarizes recent insights into the molecular mechanisms of persister formation, explains how persisters complicate antibiotic treatment of infections, and outlines emerging strategies to combat these tolerant cells.



中文翻译:

细菌持久性的分子机制和临床意义

任何细菌种群都具有少量的表型变异体,这些变异体在暴露于高浓度抗生素后仍能幸免。重要的是,这些所谓的“持久性细胞”损害了细菌感染的成功抗生素治疗,并被认为有助于抗生素耐药性的发展。有趣的是,药物耐受性持久剂也已被确定为肿瘤细胞群中化疗失败的潜在因素。最近的研究已经开始揭示持久性物质形成的复杂分子机制,并围绕应激反应和毒素-抗毒素模块展开。此外,在体外进化实验揭示了对该表型的进化和适应性方面的见识。此外,不断改进的实验技术正在刺激人们在其与感染相关的自然体内环境中研究持久性蛋白的努力。这篇综述总结了对持久性形成的分子机制的最新见解,解释了持久性如何使感染的抗生素治疗复杂化,并概述了对抗这些耐受细胞的新兴策略。

更新日期:2016-10-15
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