感染SARS-CoV-2诱导HMGB1通过转化后修饰和PANoptosis的分泌
Man Sup Kwak1,2, Seoyeon Choi1,3, Jiseon Kim3,4
1Department of Microbiology, Yonsei University College of Medicine, Seoul 03722, Korea.
Immune network
|July 7, 2023
概括
严重急性呼吸道综合征冠状病毒2 (SARS-CoV-2) 感染触发高流动性组盒1 (HMGB1) 通过主动和被动途径释放. 一种新的细胞死亡形式PANoptosis与SARS-CoV-2感染期间的HMGB1被动释放有关.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 病毒学 病毒学
背景情况:
- 严重急性呼吸系统综合征冠状病毒2 (SARS-CoV-2) 感染导致严重的炎症和器官损伤.
- 高流动性组盒1 (HMGB1),一种与损伤相关的分子模式,与炎症性疾病有关.
- HMGB1分泌与促炎性刺激和病毒感染有关.
研究的目的:
- 为了研究SARS-CoV-2感染期间HMGB1分泌的机制.
- 确定是否涉及主动和被动释放通路.
- 探索 PANoptosis 在 HMGB1 释放中的作用.
主要方法:
- 使用HEK293E/ACE2-C-GFP和Calu-3细胞系进行体外研究.
- 分析了HMGB1.1的翻译后修改 (乙化,酸化,氧化).
- 在人类和小鼠的肺组织中使用免疫组织化学和免疫光学.
主要成果:
- 通过翻译后的修改,SARS-CoV-2感染诱导了HMGB1的活性分泌.
- 证明PANoptosis是SARS-CoV-2感染期间HMGB1被动释放的新途径.
- 在受感染的人类和小鼠肺组织中确认了HMGB1的转移和释放.
结论:
- HMGB1分泌是SARS-CoV-2病变发生的一个关键事件.
- 活跃的HMGB1释放涉及特定的翻译后修改.
- 泛光死在被动HMGB1释放中发挥关键作用,导致SARS-CoV-2引起的炎症和损伤.
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