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IL-1β改变了泌尿病原性大肠杆菌的毒性
Fatma Kalaycı-Yüksek1, Rongrong Wu2, Ignacio Rangel2
1Faculty of Medicine, Department of Medical Microbiology, Istanbul Yeni Yüzyıl University, Istanbul, Turkey.
Scientific reports
|October 30, 2025
概括
促炎性细胞因子IL-1β通过改变其新陈代谢来增强尿病原性大肠杆菌 (UPEC) 的毒性. 这种新陈代谢转变促进了UPEC的增强.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 宿主-病原体相互作用
背景情况:
- 泌尿病原性大肠杆菌 (UPEC) 是尿路感染 (UTI) 的主要原因之一.
- 研究了宿主对UPEC的免疫反应,但宿主细胞因子对UPEC毒性的影响不太清楚.
研究的目的:
- 研究促炎性细胞因子IL-1β如何影响UPEC毒性,新陈代谢和宿主-病原体相互作用.
- 阐明IL-1β影响UPEC的机制.
主要方法:
- UPEC菌株CFT073对IL-1β的暴露.
- 测量氧气消耗率 (OCR) 和细胞外酸化率 (ECAR),以评估代谢变化.
- 微阵列分析以确定基因表达变化.
- 在膀上皮细胞中评估UPEC粘附和入侵.
- 使用C. elegans感染模型评估UPEC与宿主相互作用.
主要成果:
- 暴露于IL-1β诱导了UPEC从呼吸到发酵的代谢转变 (降低了OCR,增加了ECAR).
- 观察到发酵性 (hyc) 和抗氧化剂 (katG,ahpF,grxA) 基因的升级,以及 purin 生物合成的增加.
- 通过上调 fimH 和 papC 基因表达,IL-1β 增加了 UPEC 的粘附和侵入.
- 在C. elegans模型中,IL-1β刺激的UPEC抑制了先天免疫基因表达.
结论:
- 在UPEC中,IL-1β诱导了一种增强毒性的代谢适应.
- 这种新陈代谢重编程可能会促进UPEC的持久性和尿道中的殖民化.
- IL-1β和UPEC之间的跨王国信号传递对尿路感染病原发生有影响.
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