HMGB1
坏死性下垂
上睑下垂
分泌物
程序性细胞死亡
细胞外
炎症
促炎细胞因子
医学
细胞激素风暴
免疫学
细胞凋亡
生物
细胞生物学
炎症体
2019年冠状病毒病(COVID-19)
内科学
传染病(医学专业)
疾病
生物化学
作者
Man Sup Kwak,Seong-Jin Choi,Jiseon Kim,Hoojung Lee,Inho Park,Jooyeon Oh,Duong Tran Ngoc,Nam Hyuk Cho,Ki Taek Nam,Jeon-Soo Shin
出处
期刊:Immune Network
[Korean Association of Immunobiologists]
日期:2023-01-01
卷期号:23 (3)
被引量:6
标识
DOI:10.4110/in.2023.23.e26
摘要
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection induces excessive pro-inflammatory cytokine release and cell death, leading to organ damage and mortality. High-mobility group box 1 (HMGB1) is one of the damage-associated molecular patterns that can be secreted by pro-inflammatory stimuli, including viral infections, and its excessive secretion levels are related to a variety of inflammatory diseases. Here, the aim of the study was to show that SARS-CoV-2 infection induced HMGB1 secretion via active and passive release. Active HMGB1 secretion was mediated by post-translational modifications, such as acetylation, phosphorylation, and oxidation in HEK293E/ACE2-C-GFP and Calu-3 cells during SARS-CoV-2 infection. Passive release of HMGB1 has been linked to various types of cell death; however, we demonstrated for the first time that PANoptosis, which integrates other cell death pathways, including pyroptosis, apoptosis, and necroptosis, is related to passive HMGB1 release during SARS-CoV-2 infection. In addition, cytoplasmic translocation and extracellular secretion or release of HMGB1 were confirmed via immunohistochemistry and immunofluorescence in the lung tissues of humans and angiotensin-converting enzyme 2-overexpressing mice infected with SARS-CoV-2.
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