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NLRP6炎症酶识别脂铁醇酸并调节格兰美阳性病原体感染

Hideki Hara¹, Sergey S Seregin², Dahai Yang¹

¹Department of Pathology and Rogel Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

|November 6, 2018

概括

利波泰可酸 (LTA) 激活NLRP6炎症体,从而启动先天免疫反应. 这种途径涉及酶-11和素-18 (IL-18),加剧了Gram阳性细菌感染.

科学领域:

免疫学
微生物学
细胞生物学

背景情况:

目前尚不完全了解NLRP6炎症酶的激活剂和功能.
具有已知的免疫调节作用的成分.

研究的目的:

为了确定NLRP6炎症酶的激活剂.
阐明NLRP6在对格拉姆阳性细菌感染的天生的免疫力中的作用.

主要方法:

研究了巨细胞中NLRP6的LTA结合和激活.
使用NLRP6淘汰 (NLRP6-/-) 和Casp11淘汰 (Casp11-/-) 的小鼠模型.
评估了对Listeria monocytogenes感染的敏感性,并测量了细胞因子的产生.

主要成果:

利波泰可酸 (LTA) 直接结合并激活NLRP6.
激活NLRP6导致酶-11和酶-1的招募,促进IL-1β和IL-18的成熟.
Nlrp6-/-和Casp11-/-小鼠对L. monocytogenes感染的易感性降低,病原体负载较低,IL-18的产生受损.
在NLRP6或Casp11小鼠中,IL-18的使用恢复了敏感性.

结论:

细胞质LTA是格拉姆阳性细菌的关键组成部分,它激活NLRP6.
这种LTA-NLRP6-caspase-11通路驱动IL-18的产生,加剧了全身Gram阳性细菌感染.
这些发现揭示了一种对宿主防御和病原体控制至关重要的新生免疫路径.

关键词:

一个IL-18 李斯特菌单细胞菌在NLRP6 卡斯帕斯-1 卡斯帕斯- 11 阳性细菌炎症组利波泰可酸

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