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胆酸受体Tgr5通过代谢和表观遗传沉默防止细菌败血症期间的巨细胞过度炎症

Maria Reich¹, Tobias Franz², Haifeng C Xu³

¹Department of Gastroenterology, Hepatology and Infectious Diseases, University Hospital Magdeburg, Medical Faculty, Otto-von-Guericke University, 39120 Magdeburg, Germany.

|December 11, 2025

概括

塔凯达的G蛋白结合受体5 (Tgr5) 通常会平静免疫细胞. 然而,巨细胞中的Tgr5缺乏导致过度活跃的炎症和增加对Listeria monocytogenes败血症的易感性.

科学领域:

免疫学免疫学免疫学
代谢途径代谢途径
微生物的病原发生.

背景情况:

塔克达G蛋白结合受体5 (Tgr5) 是一种已知调节免疫细胞的胆酸受体.
Tgr5影响免疫反应的精确分子机制尚不清楚.

研究的目的:

研究Tgr5在细菌感染期间巨细胞炎症反应中的作用.
阐明将Tgr5信号与免疫细胞功能和代谢调节联系起来的分子机制.

主要方法:

使用Listeria monocytogenes进行巨细胞刺激.
对Tgr5表达水平的分析.
评估Tgr5缺乏的巨细胞中的炎症标志物.
代谢分析包括糖解和ATP酸酶表达的分析.
在患有骨髓Tgr5缺乏症的小鼠中对Listeria monocytogenes败血症敏感性的评估.

主要成果:

在Listeria monocytogenes刺激后,Tgr5表达在巨细胞中被上调.
缺乏Tgr5的巨细胞表现出高度的炎症反应.
缺乏髓质Tgr5的小鼠对Listeria monocytogenes败血症的敏感性增加.
缺少Tgr5导致糖解和ATP酸酶表达减少,导致乙-CoA缺乏.
缺陷的代谢-表观遗传基因沉默有助于Tgr5缺陷巨细胞中的超炎症表型.

结论:

在细菌败血症期间,Tgr5在调节巨细胞炎症反应方面发挥着关键作用.
Tgr5信号与代谢途径密切相关,特别是糖解和乙-CoA生产.
调节失调的Tgr5-介导的代谢控制驱动高炎症和恶化败血症的结果.

关键词:

生物科学生物科学免疫学免疫学免疫学微生物学的微生物.自然科学自然科学自然科学

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