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Cell wall deficiency as an escape mechanism from phage infection
Open Biology ( IF 4.5 ) Pub Date : 2021-09-01 , DOI: 10.1098/rsob.210199
Véronique Ongenae 1, 2 , Ariane Briegel 1, 2 , Dennis Claessen 1, 2
Affiliation  

The cell wall plays a central role in protecting bacteria from some environmental stresses, but not against all. In fact, in some cases, an elaborate cell envelope may even render the cell more vulnerable. For example, it contains molecules or complexes that bacteriophages recognize as the first step of host invasion, such as proteins and sugars, or cell appendages such as pili or flagella. In order to counteract phages, bacteria have evolved multiple escape mechanisms, such as restriction-modification, abortive infection, CRISPR/Cas systems or phage inhibitors. In this perspective review, we present the hypothesis that bacteria may have additional means to escape phage attack. Some bacteria are known to be able to shed their cell wall in response to environmental stresses, yielding cells that transiently lack a cell wall. In this wall-less state, the bacteria may be temporarily protected against phages, since they lack the essential entities that are necessary for phage binding and infection. Given that cell wall deficiency can be triggered by clinically administered antibiotics, phage escape could be an unwanted consequence that limits the use of phage therapy for treating stubborn infections.



中文翻译:


细胞壁缺陷作为噬菌体感染的逃避机制



细胞壁在保护细菌免受某些环境压力(但并非所有环境压力)方面发挥着核心作用。事实上,在某些情况下,复杂的细胞包膜甚至可能使细胞更加脆弱。例如,它含有噬菌体识别为宿主入侵第一步的分子或复合物,例如蛋白质和糖,或细胞附属物,例如菌毛或鞭毛。为了对抗噬菌体,细菌进化出了多种逃逸机制,例如限制性修饰、流产感染、CRISPR/Cas系统或噬菌体抑制剂。在这篇综述中,我们提出了这样的假设:细菌可能有其他方法来逃避噬菌体的攻击。已知一些细菌能够响应环境压力而脱落细胞壁,产生暂时缺乏细胞壁的细胞。在这种无壁状态下,细菌可以暂时免受噬菌体的侵害,因为它们缺乏噬菌体结合和感染所需的基本实体。鉴于临床使用的抗生素可能引发细胞壁缺陷,噬菌体逃逸可能是一种不良后果,限制了噬菌体疗法在治疗顽固感染中的应用。

更新日期:2021-09-01
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