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在抗生素治疗期间,沙门氏菌持续破坏宿主免疫防御

Daphne A C Stapels¹, Peter W S Hill¹, Alexander J Westermann^2,3

¹MRC Centre for Molecular Bacteriology and Infection, Imperial College London, London, UK.

Science (New York, N.Y.)

|December 8, 2018

概括

沙门氏菌在巨细胞内持续存在, 保持活跃, 重新编程免疫细胞, 这种免疫规避有助于抗生素治疗后的细菌复发.

科学领域:

微生物学
免疫学
细菌致病性

背景情况:

抗生素耐受性的持续细胞有助于持续和复发的细菌感染.
持久性细胞通常被认为是休眠的,但它们在宿主细胞 (如巨细胞) 中的状态尚不清楚.

研究的目的:

在巨感染期间调查沙门氏菌的生理状态.
阐明这些持久细胞在巨细胞内生存的机制.

主要方法:

在受感染的巨细胞中分析沙门氏菌的持续细胞活动.
研究由沙门氏病原性岛2型3分泌系统分泌的效应蛋白.
评估巨细胞的免疫反应和两极化.

主要成果:

在巨细胞内存在的沙门氏菌是代谢活跃的,而不是休眠的.
分泌的效应物重编程巨细胞,抑制炎症并促进抗炎两极分化.
这种重新编程有助于非生长型沙门氏菌的长期存活.

结论:

沙门氏菌持续活跃地操纵宿主巨细胞以求生存.
耐性菌的免疫重编程是细菌持续性和潜在复发的关键因素.
针对持久性宿主相互作用可能提供新的治疗策略.

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