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Plausible role of bacterial toxin-antitoxin system in persister cell formation and elimination.
Molecular Oral Microbiology ( IF 2.8 ) Pub Date : 2019-05-02 , DOI: 10.1111/omi.12258
Prajita Paul 1 , Bikash R Sahu 1 , Mrutyunjay Suar 1
Affiliation  

Although, a large proportion of pathogenic bacteria gets eliminated from hosts after antibiotic treatment, a fraction of population confronts against such effects and undergoes growth arrest to form persisters. Persistence in bacteria is a dormant physiological state where cells escape the effects of antimicrobials as well as other host immune defences without any genetic mutations. The state of dormancy is achieved through various complex phenomena and it is known that a gene pair named as toxin–antitoxin (TA) acts as a key player of persister cell formation where the toxin is activated either stochastically or after an environmental insult, thereby silencing the physiological processes. However, the controversial role of TA modules in persister cell formation has also been documented with reasonable clarity. Persisters may revert back from state of quiescence and regrow when conditions become favourable for their propagation. Therefore, the elimination of dormant bacteria is crucial, and currently, research interest is highly focussed on developing several antipersister strategies that may kill persister bacteria by targeting different molecules. It is worth examining these targets to develop appropriate therapeutic interventions against bacterial infections and it is believed that earmarking TA system can be a novel approach for resuscitation of persisters. In this review, we discussed the role of TA modules in mediating persistence with highlighting on the debatable issues regarding contribution of these modules in dormant bacteria formation. Furthermore, we discussed if these modules in bacteria can be targeted for successful elimination of dormant persister cells.

中文翻译:

细菌毒素-抗毒素系统在持续性细胞形成和消除中的合理作用。

尽管在抗生素治疗后,大部分致病菌已从宿主中清除,但仍有一部分人口面临这种影响,并经历了生长停滞而形成了持久性细菌。细菌的持久性是一种休眠的生理状态,在这种状态下,细胞可以逃脱抗微生物剂以及其他宿主免疫防御的作用而没有任何基因突变。休眠状态是通过各种复杂的现象来实现的,已知一种名为毒素-抗毒素(TA)的基因对可作为持久性细胞形成的关键参与者,在该过程中,毒素被随机激活或在受到环境破坏后被激活,从而沉默生理过程。但是,TA模块在持久性细胞形成中的有争议作用也已经以合理的清晰度得到了证明。当条件变得有利于繁殖时,波斯人可能会从静止状态恢复原状并重新生长。因此,消除休眠细菌是至关重要的,目前,研究兴趣高度集中在开发几种可通过靶向不同分子来杀死持久性细菌的抗杀虫剂策略上。值得研究这些目标以开发针对细菌感染的适当治疗性干预措施,并且相信指定TA系统可以成为复苏持续性疾病的新方法。在这篇综述中,我们讨论了TA模块在介导持久性中的作用,重点介绍了有关这些模块在休眠细菌形成中的作用的有争议的问题。此外,我们讨论了细菌中的这些模块是否可以靶向成功消除休眠的持久性细胞。
更新日期:2019-05-02
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