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在患有严重SARS-CoV-2感染的患者中,编程细胞死亡的差异激活
Ashleigh N Riegler1, Paul Benson2, Kenneth Long3
1Division of Laboratory Medicine, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
Cell death discovery
|November 21, 2023
概括
严重的SARS-CoV-2感染会增加肺部的热和死. 亡与病毒载量有很强的相关性,这表明SARS-CoV-2的直接机制,而亡似乎是由炎症驱动的.
科学领域:
- 病理学 病理学 病理学
- 免疫学 免疫学 免疫学
- 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) 导致严重的肺部疾病.
- 了解SARS-CoV-2肺病理中的编程细胞死亡 (PCD) 作用至关重要,但有限.
- 现有的知识依赖于小型解剖研究,体外和动物模型.
研究的目的:
- 在SARS-CoV-2感染的人类肺部中识别,定位和量化apoptosis,ferroptosis,pyroptosis和necroptosis.
- 在严重的SARS-CoV-2感染中,将PCD激活与病毒负担相关联.
- 阐明在SARS-CoV-2肺病理学中驱动PCD的机制.
主要方法:
- 分析了28名SARS-CoV-2患者和13名对照组的FFPE肺组织.
- 针对SARS-CoV-2核蛋白和PCD标记物的免疫光 (IF) 染色 (切割的Caspase-3,pMLKL,切割的Gasdermin D,CD71).
- 全幻灯片成像和Image J软件用于量化和定位.
主要成果:
- 亡和铁亡在感染肺和控制肺之间没有显著差异.
- 在SARS-CoV-2感染的肺部中,亡和亡都显著增加.
- 不管病毒载量如何,火灭菌的增加,这表明炎症驱动的激活.
- 亡与病毒负担有很强的相关性 (R2 = 0.9925),表明直接的SARS-CoV-2影响.
结论:
- SARS-CoV-2 感染差异地激活了肺部编程的细胞死亡途径.
- 烧死和亡,但不是亡或铁亡,是涉及SARS-CoV-2肺病理的关键液性PCD途径.
- 亡可能由SARS-CoV-2直接调解,而亡可能是由炎症驱动的.
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