TisB通过防止通过ATP枯竭的prophage诱导使沙门氏菌能够耐受抗生素
Sebastian Braetz1, Niclas Nordholt2, Andreas Nerlich3
1Institute of Microbiology and Epizootics, School of Veterinary Medicine, Freie Universität Berlin, Berlin, Germany.
PLoS pathogens
|September 22, 2025
概括
低细胞内ATP水平增加细菌的抗生素持久性,通过抑制prophage诱导. 菌体激活对于DNA损伤中介杀死至关重要,在抗生素治疗后的恢复增强了菌体诱导.
科学领域:
- 微生物学 微生物学
- 细菌生理学 细菌生理学
- 抗生素耐药性 抗生素耐药性
背景情况:
- 持久性细胞是耐抗生素的细菌,在没有耐药性的情况下存活在治疗中.
- 低细胞内ATP水平被假设通过减少抗生素向活性,有助于持续性.
- 已被证明,内源性prophages在暴露于诺基诺后可以降低沙门氏菌的持久性.
研究的目的:
- 为了调查prophage诱导和ATP水平在细菌持久性中的作用.
- 检查tisAB毒素-抗毒素系统对沙门氏菌Typhimurium持久性和prophage活动的影响.
- 为了确定恢复阶段对菌诱导和细菌存活的影响.
主要方法:
- 使用了一种无菌的沙门氏菌Typhimurium变种和一个tisAB删除菌株.
- 暴露于西普洛素的细菌菌株,以评估杀死和持久性.
- 监测在抗生素治疗期间和之后的prophage诱导和ATP水平.
主要成果:
- 与野生型沙门氏菌相比,一种无菌变体的杀死率降低,持久性增加.
- 删除tisAB显著增加了在治疗西普罗夫洛克萨后的prophage诱导和杀死.
- 齐普罗夫洛克萨后的恢复阶段对于内源性prophage诱导至关重要.
结论:
- 在DNA损伤中介的细菌杀死中,依赖ATP的prophage激活至关重要.
- 细胞内ATP水平降低抑制了prophage诱导,导致在治疗后的生存率更高.
- 向ATP水平或传播途径可能为抗生素持久性提供新的策略.
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