沙门氏菌抗毒素DinJ抑制了巨细胞中NLRP3依赖的正规炎症酶激活
Dan Gu1,2,3, Ang Li1,2,3, Xirui Zang1,2,3
1Jiangsu Key Laboratory of Zoonosis/Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou, Jiangsu, China.
Infection and immunity
|March 13, 2024
概括
沙门氏菌 (Salmonella Enteritidis DinJ) 抑制炎症酶激活,这是天生的免疫系统的关键组成部分. 这种细菌蛋白质有助于沙门氏菌通过抑制IL-1β和IL-18分泌来逃避宿主免疫清除.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 分子生物学分子生物学
背景情况:
- 炎症酶对抗微生物感染的天生的免疫力至关重要.
- 沙门氏菌 (Salmonella Enteritidis) 采用策略,通过调节炎症酶激活来逃避宿主免疫反应.
研究的目的:
- 调查Salmonella Enteritidis中的抗毒素DinJ在调节炎酶激活和宿主免疫逃避中的作用.
主要方法:
- 查Salmonella Enteritidis转子突变库以确定影响炎症酶激活的基因.
- 基因分析,包括删除突变体 (ΔfliCΔdinJ) 和共同转录确认.
- 基于细胞的测试使用J774A.1细胞和主要骨髓衍生巨细胞 (BMDMs).
- 对于切割的Caspase-1和IL-1β.的西部涂抹.
- 光共振能量转移 (FRET) 用于DinJ转位.
- 在体内研究评估IL-1β和IL-18分泌.
主要成果:
- 插入突变dinJ增加了沙门氏菌Enteritidis中的炎症酶激活.
- 删除突变 ΔfliCΔdinJ 增强了细胞死亡和 IL-1β 分泌.
- 证实DinJ在BMDM中抑制了正规炎症酶激活,特别是NLRP3.
- 在感染期间,FRET证实了DinJ转移到宿主细胞.
- 在体内,DinJ抑制了IL-1β和IL-18的分泌,有助于细菌的免疫逃避.
结论:
- 丁作为常规炎症酶激活的抑制剂,特别是NLRP3.
- 丁通过抑制宿主炎症反应,有助于沙门氏菌菌的免疫逃避.
- 这项研究阐明了一种由DinJ介导的细菌免疫逃避的新机制.
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