通过与NLRC4/NAIP炎症酶的直接相互作用,T3SS转位子会诱导热
Yan Zhao1,2, Hanshuo Zhu1,3,4, Jinqian Li2,5
1CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Institute of Oceanology; CAS Center for Ocean Mega-Science, Chinese Academy of Sciences, Qingdao, China.
eLife
|February 14, 2025
概括
来自Edwardsiella tarda的转位蛋白 EseB 触发了 NLRC4 炎症酶介导的灭. 这种保存的机制突出显示了细菌的III型分泌系统如何激活宿主细胞死亡途径.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 第三类分泌系统 (T3SS) 是许多细菌病原体的关键毒性因子,促进了效应蛋白的注入宿主细胞.
- NLRC4炎症体是T3SS组件的关键传感器,主要是针和基底棒蛋白,启动炎症反应.
- 其他T3SS组件,如转位子,在炎症酶激活中的精确作用仍然不完全理解.
研究的目的:
- 用*Edwardsiella tarda*作为模型研究T3SS和宿主炎症细胞通路之间的相互作用.
- 阐明T3SS组件,特别是转位子,诱导宿主细胞死亡的分子机制.
- 为了确定观察到的炎酶激活机制是否在不同的细菌病原体中保持.
主要方法:
- 利用*Edwardsiella tarda*作为一种模型细胞内病原体来研究T3SS-宿主炎症体相互作用.
- 评估了在宿主细胞中依赖T3SS组件和炎症蛋白质 (NLRC4,NLRP3,ASC,caspase1/4) 的烧灭酶诱导.
- 研究了转位蛋白Eseb与NAIP的结合,并确定了NLRC4激活的关键C终端区域 (T6R).
主要成果:
- *E. tarda*诱导的热需要细菌的转位和宿主炎症组分NLRC4,NLRP3,ASC和caspase 1/4.4.
- 转位蛋白EseB通过其C端6残留物 (T6R) 与NAIP相互作用,直接触发NLRC4/NAIP介导的热.
- 在T3SS阳性细菌中广泛存在的EseB同类物,在T6R区域共享高序列相同性,并表现出保留的T6R依赖的NLRC4激活能力.
结论:
- 转位蛋白EseB在通过NLRC4炎症酶激活来启动宿主细胞热中发挥着至关重要的作用.
- 埃塞B的C端区域 (T6R) 对于NAIP结合和随后的炎症酶激活至关重要,代表了一个保存的机制.
- 这项研究揭示了一种保存的分子机制,T3SS转位子激活细菌病原体中的炎症体,提供了对宿主-病原体相互作用的见解.
关键词:
在NLRC4中,这就是T3SS.人类 人类 人类 人类 人类 人类 人类免疫学 免疫学 免疫学传染病是一种传染性疾病.这是一种炎症炎症炎症炎症.微生物学的微生物.病原体与宿主相互作用跨局面的跨局面更多相关视频
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