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NOD2通过增加由LACC1介导的大脑内质网膜压力来促进败血症诱导的神经炎症

Lingling Yi¹, Zhuo Chen¹, Qiuping Zhou²

¹School of Medicine, South China University of Technology, Guangzhou, 510006, Guangdong Province, China; Department of Critical Care Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510080, Guangdong Province, China.

Free radical biology & medicine

|May 7, 2025

概括

含有核酸结合寡合化域的蛋白2 (NOD2) 通过LACC1.1通过增加内 плазма网膜 (ER) 应激,促进败血症诱导的神经炎症. 抑制NOD2或LACC1可能为神经炎症提供新的治疗方法.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

核酸结合寡聚化域含蛋白2 (NOD2) 在败血症诱导的神经炎症中的作用在很大程度上是未知的.
NOD2与各种炎症状况和一些神经系统疾病有关.

研究的目的:

研究NOD2在败血症引起的神经炎症中的作用.
阐明NOD2影响神经炎症的潜在机制.

主要方法:

在小鼠模型和微质细胞中分析了NOD2表达.
产生了NOD2淘汰赛小鼠,并接受了结和穿孔 (CLP) 诱导败血症.
试验室研究涉及siRNA介导的NOD2和LACC1的淘汰,以及使用ER压力抑制剂的治疗.
评估神经炎症和ER压力使用免疫光学,西部涂抹和qPCR.

主要成果:

在败血症诱导的神经炎症期间,NOD2表达被上调.
缺少NOD2可以保护神经炎症,这与减少ER压力有关.
含有甲基酶域的蛋白1 (LACC1) 被确定为ER压力和神经炎症恶化的关键调解者.
NOD2通过LACC1增强了ER压力和神经炎症,LACC1下调部分扭转了这一效应.

结论:

NOD2通过调节LACC1.1介导的ER压力,在促进败血症诱导的神经炎症方面发挥着关键作用.
准NOD2-LACC1-ER应激通路为神经炎症提供了一个潜在的治疗策略.

关键词:

细胞内膜网膜应激压力含有甲基酶域的蛋白1 (LACC1)微质细胞中的微质细胞含有核酸结合寡合化域的蛋白2 (NOD2)败血症诱导的神经炎症

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