两个组件系统HprS/HprR通过增加鞭毛体表达来增强尿病原菌大肠杆菌CFT073的脏殖民
Xueping Li1, Yu Pang2, Zixiang Liu1
1School of Life Sciences, Tianjin University, Tianjin 300072, P.R. China; State Key Laboratory of Synthetic Biology, Tianjin University, Tianjin 300072, P.R. China.
Cell reports
|February 1, 2026
概括
一个由两个组成部分组成的系统,HprSR,激活了尿路病原性大肠杆菌 (UPEC) 中的鞭毛基因表达. 这促进了脏殖民,使细菌在对主体反应性氧和物种的反应中具有运动性.
科学领域:
- 微生物学 微生物学
- 病变的发生和发病.
- 分子生物学分子生物学
背景情况:
- 尿路感染 (UTI) 主要是由通过上升感染引起的尿病原菌大肠杆菌 (UPEC) 引起的.
- UPEC侵入膀并上升到脏,导致皮叶龙炎,其鞭毛介导的运动性对传播至关重要.
- 在对宿主线索的反应中控制鞭毛基因表达的调控机制尚未完全理解.
研究的目的:
- 在UPEC中阐明控制鞭毛基因表达的调节途径.
- 为了研究HprSR双组件系统在UPEC殖民中的作用.
- 为了确定宿主衍生反应性物种如何影响UPEC毒性.
主要方法:
- 研究了由HprSR双组件系统直接激活fliLMNOPQR操作子的情况.
- 利用突变分析 (hprSR突变) 来评估对UPEC殖民的影响.
- 研究了中和宿主衍生反应性氧物种 (ROS) 和反应性物种 (RCS) 对UPEC殖民的影响.
主要成果:
- 该HprSR系统直接激活fliLMNOPQR操作子,这对于鞭毛的运动性至关重要.
- hprSR突变显著损害了UPEC脏的殖民化,由于减少了鞭毛基因表达.
- 在体内中和ROS和RCS的中和,通过使HprSR.不活化来防止UPEC脏殖民.
结论:
- 两个组成部分的HprSR系统是UPEC鞭毛细胞运动和毒性的关键调节器.
- 来自宿主的ROS和RCS激活HprSR,促进UPEC脏殖民.
- 这项研究揭示了一种关键的宿主-病原体相互作用途径,可以调解尿路感染病原体.
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