来自Enterococcus faecalis的乳酸抑制了巨细胞的激活,以促进持久性和多微生物伤口感染
Ronni A G da Silva1, Brenda Yin Qi Tien2, Patrick Hsien Neng Kao2
1Singapore-MIT Alliance for Research and Technology Centre, Antimicrobial Resistance Interdisciplinary Research Group, Singapore, Singapore; Singapore Centre for Environmental Life Sciences Engineering, Nanyang Technological University, 60 Nanyang Drive, Singapore 637551, Singapore.
Cell host & microbe
|January 28, 2026
概括
Enterococcus faecalis通过释放乳酸来抑制天生的免疫力,乳酸会使环境酸化并抑制巨细胞的激活. 这种细菌机制促进了持续的感染,并有助于共感染病原体.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 生物化学 生物化学
背景情况:
- 巨细胞的激活对于有效的先天免疫和对抗微生物感染至关重要.
- 病原细菌经常采用复杂的策略来逃避宿主免疫反应,并建立持久的感染.
研究的目的:
- 阐明Enterococcus faecalis抑制巨细胞激活的机制.
- 调查乳酸在调解E. faecalis.免疫逃避中的作用.
- 了解细菌免疫抑制如何影响慢性和多微生物感染.
主要方法:
- 研究了乳酸在抑制巨细胞激活中的作用,使用E. faecalis.
- 利用单碳酸盐载体1 (MCT-1) 和GPR81信号通路来研究免疫抑制.
- 评估了细菌乳酸盐生产对NF-κB信号传递和免疫细胞功能的影响.
- 采用小鼠伤口感染模型来评估乳酸介导免疫抑制的体内意义.
主要成果:
- Enterococcus faecalis通过乳酸介导的细胞外酸化抑制了巨细胞的激活.
- 细菌乳酸通过MCT-1和GPR81起作用,抑制核因子 κB (NF-κB) 信号传递.
- 乳酸降低了MyD88水平,并诱导了YAP酸化,共同减弱了NF-κB.
- 一种E. faecalis的乳酸脱酶突变未能抑制NF-κB,证实了乳酸的作用.
- 在体内以乳酸驱动的免疫抑制促进了E. faecalis的持久性,并增强了共感染细菌的适应性.
结论:
- 细菌乳酸是一种关键的毒性因子,通过抑制巨细胞激活来颠覆天生的免疫力.
- 鉴定到的E. faecalis免疫抑制机制有助于病原体的持久性和多微生物感染.
- 准细菌的乳酸生产或其下游信号通路可能为治疗慢性感染提供治疗策略.
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