黄金葡萄球菌 (Staphylococcus aureus) 载体AbcA增强了在β-乳酸暴露下持久形成的作用
Q C Truong-Bolduc1, Y Wang1, R Ferrer-Espada2
1Infectious Diseases Division and Medical Services, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Antimicrobial agents and chemotherapy
|February 16, 2024
概括
黄金葡萄球菌的持久性细胞通过过度表达AbcA转运体而在抗生素中存活,该转运体可以出纳夫西林,但不能出氧西林. 这种排泄活动提高了抗生素治疗期间的细菌存活率.
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:
- 细菌的持久性是导致复发性感染和治疗失败的关键因素.
- 持续性细胞形成和生存背后的机制仍然不完全理解.
- 溢出与抗菌素耐药性有关,但它们在细菌持久性中的作用需要进一步阐明.
研究的目的:
- 研究黄金葡萄球菌 (Staphylococcus aureus AbcA) 载体在细菌持久性和生存中的作用.
- 为了确定AbcA表达是否与对纳弗西林和西林的耐药性相关.
- 评估AbcA对在人群和单细胞水平上持续细胞形成和生存的贡献.
主要方法:
- 使用光记者来监测细胞活力和ABCA表达.
- 使用共聚焦显微镜对表达AbcA的细胞进行种群级分析.
- 使用高通量微流体系统进行单细胞分析.
- 生成并测试一个abcA淘汰突变体对抗生素敏感性.
主要成果:
- 过度表达AbcA给纳夫西林带来了耐药性,而不是氧西林.
- 在持久性形成期间观察到AbcA记者阳性细胞的六倍增加,因为细胞活力下降.
- 单细胞分析显示,抗生素暴露与ABCA记者表达之间存在强烈的相关性.
- 该abcA绝杀突变体在暴露于纳夫西林后显示了持续细胞水平的降低.
- 纳夫西林和西林治疗的幸存者始终表达过度的AbcA.
结论:
- 该ABCA排泄通过积极抽出纳夫西林,有助于黄金葡萄球菌的生存.
- 在使用基抗生素 (如纳夫西林) 治疗期间,由abcA介导的流量选择性地丰富了持久种群.
- 流量活动,特别是AbcA,在细菌持续细胞的生存中起着重要作用.
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