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S100a9 保护反复社会失败,压力和压力的影响

Cassandra M Moshfegh¹, Safwan K Elkhatib¹, Gabrielle F Watson^1,2

¹Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska.

Biological psychiatry global open science

|October 26, 2023

概括

心理创伤后高调节的蛋白质calprotectin在遗传上被删除时,令人惊的是会使创伤后应激障碍症状恶化. 失去calprotectin会加剧T细胞的炎症和线粒体功能障碍.

科学领域:

神经免疫学神经免疫学
细胞生物学细胞生物学
线粒体生物学线粒体生物学

背景情况:

创伤后应激障碍 (PTSD) 与炎症和炎症性疾病风险增加有关.
连接PTSD和炎症的确切机制尚未完全理解.
编码calprotectin的S100a8和S100a9基因在创伤后的T淋巴细胞中被上调,与炎症和氧化还原状态相关联.

研究的目的:

调查calprotectin在PTSD相关的炎症和氧化还原变化的作用.
测试假设,calprotectin的遗传删除会减轻与PTSD相关的表型.

主要方法:

利用PTSD (重复社会失败压力 - RSDS) 的小鼠模型.
使用基因操纵来消除calprotectin (S100a9删除).
分析了行为,炎症和细胞氧化还原特征,包括单细胞RNA测序.

主要成果:

与假设相反,calprotectin删除恶化了RSDS后的行为病理,炎症和线粒体氧化还原环境.
失去了calprotectin增加了对T淋巴细胞的代谢需求.
单细胞RNA测序揭示了线粒体功能和氧化酸化途径的显著改变.

结论:

失去了calprotectin增强了PTSD诱导的表型,表明具有保护作用.
在心理创伤后,calprotectin的升级可能会提供以前未知的保护功能.
卡尔蛋白蛋白可能在T淋巴细胞中调节线粒体功能的过程中起到未经表征的作用.

关键词:

在 Calprotectin 中使用.炎症炎症是一种炎症.代谢过程中的代谢.线粒体中的线粒体.氧化还原剂的使用方法这是T淋巴细胞.

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