致命的COVID-19与RAAS诱导的多器官损伤的炎症有关,包括中间骨淋巴结
Michael J Topper1,2, Joseph W Guarnieri1,3,4, Jeffrey A Haltom1,3,4
1COVID-19 International Research Team, Medford, MA 02155.
概括
致命的COVID-19涉及一个重新定义的细胞因子风暴,由免疫基因和线粒体信号驱动. 这导致氨酸- ангиотензин- алдостерон系统过度激活,器官损伤和淋巴结功能受损.
科学领域:
- 免疫学 免疫学 免疫学
- 病理学 病理学 病理学
- 基因组学就是基因组学.
背景情况:
- 经典的细胞因子风暴与致命的COVID-19有关.
- 驱动严重SARS-CoV-2结果的精确机制需要进一步阐明.
研究的目的:
- 用分子和组织分析重新检查致命的COVID-19中的细胞因子风暴.
- 为了确定关键的分子通路和细胞变化,有助于致命的SARS-CoV-2感染器官损伤.
主要方法:
- 从COVID-19患者的鼻和尸检组织的RNA测序.
- 中枢淋巴结的免疫组织化学.
- 对SARS-CoV-2动物模型和人类血液样本的分析.
主要成果:
- 鼻子抽样中升级的非正规免疫基因与器官损伤相关 (心脏,肺,脏,肝脏).
- 这些基因与氨酸- ангиотензин- алдостерон系统 (RAAS) 过度激活,纤维素沉积,血管泄漏,PANoptosis 和线粒体功能障碍有关.
- 中淋巴结显示结构变化,纤维化和纤维细胞透.
结论:
- 致命的COVID-19细胞因子风暴是由上游免疫和线粒体信号驱动的.
- 这种信号激活RAAS,导致器官损伤和淋巴结功能受损.
- 研究结果与动物模型和各种SARS-CoV-2变体进行了平行比较.
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