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BRD4 调节 H.pylori 感染的巨细胞中的依赖糖解的 Nos2 表达

Nikita Modi¹, Yanheng Chen¹, Xingchen Dong¹

¹Department of Biochemistry, College of Liberal Arts & Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois.

Cellular and molecular gastroenterology and hepatology

|October 11, 2023

概括

含有基多马因的蛋白4 (BRD4) 在Helicobacter pylori感染期间调节巨细胞代谢和激活. 依赖BRD4的糖解对于氧化的产生和细菌的清除至关重要.

科学领域:

免疫学免疫学免疫学
代谢过程中的代谢.
微生物学微生物学

背景情况:

巨细胞的激活,对于天生的免疫力至关重要,涉及代谢重编程.
含原蛋白4 (BRD4) 是已知的天生的免疫反应的调节者.
在Helicobacter pylori感染期间,BRD4在巨细胞代谢重编程中的作用尚不清楚.

研究的目的:

研究BRD4在H. pylori感染期间巨细胞代谢重编程中的作用.
阐明BRD4影响巨细胞激活和细菌清除的分子机制.

主要方法:

来自野生类型和Brd4条件淘汰赛小鼠的骨髓衍生巨细胞 (BMDM) 感染了H. pylori.
用RNA测序来分析差异性基因表达.
用小鼠的体内H. pylori感染模型来验证研究结果.

主要成果:

由于BRD4的枯竭,导致H. pylori诱导的糖解和关键的糖解基因 (Slc2a1,Hk2) 的表达受损.
由缺氧诱导因子-1α招募的BRD4促进糖解并稳定No2mRNA用于氧化 (NO) 生产.
在 Brd4 缺乏的巨细胞中观察到减少了 NO 介导的 H. pylori 杀死,而 Brd4-CKO 小鼠显示胃炎症减少和细菌殖民增加.

结论:

BRD4是缺氧诱导因子-1α依赖性糖解和巨细胞激活的关键调节者.
BRD4在天生的免疫力中发挥着新的作用,通过调节糖解来稳定NO2mRNA以产生NO,帮助消除H. pylori.

关键词:

这就是BRD4D.葡萄糖溶解是什么? 葡萄糖溶解这就是H pylori.这就是HIF-1α.我们的 iNOS iNOS

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