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SARS-CoV-2 刺突蛋白激活人肺巨噬细胞。

SARS-CoV-2 Spike Protein Activates Human Lung Macrophages.

机构信息

Department of Translational Medical Sciences, University of Naples Federico II, 80131 Naples, Italy.

World Allergy Organization (WAO) Center of Excellence (CoE), 80131 Naples, Italy.

出版信息

Int J Mol Sci. 2023 Feb 3;24(3):3036. doi: 10.3390/ijms24033036.

DOI:10.3390/ijms24033036
PMID:36769357
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9917796/
Abstract

COVID-19 is a viral disease caused by SARS-CoV-2. This disease is characterized primarily, but not exclusively, by respiratory tract inflammation. SARS-CoV-2 infection relies on the binding of spike protein to ACE2 on the host cells. The virus uses the protease TMPRSS2 as an entry activator. Human lung macrophages (HLMs) are the most abundant immune cells in the lung and fulfill a variety of specialized functions mediated by the production of cytokines and chemokines. The aim of this project was to investigate the effects of spike protein on HLM activation and the expression of ACE2 and TMPRSS2 in HLMs. Spike protein induced CXCL8, IL-6, TNF-α, and IL-1β release from HLMs; promoted efficient phagocytosis; and induced dysfunction of intracellular Ca concentration by increasing lysosomal Ca content in HLMs. Microscopy experiments revealed that HLM tracking was affected by spike protein activation. Finally, HLMs constitutively expressed mRNAs for ACE2 and TMPRSS2. In conclusion, during SARS-CoV-2 infection, macrophages seem to play a key role in lung injury, resulting in immunological dysfunction and respiratory disease.

摘要

新型冠状病毒肺炎（COVID-19）是由严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）引起的病毒性疾病。这种疾病的主要特征是呼吸道炎症，但也不完全如此。SARS-CoV-2 感染依赖于刺突蛋白与宿主细胞上的血管紧张素转换酶 2（ACE2）结合。该病毒利用蛋白酶 TMPRSS2 作为进入激活剂。人肺巨噬细胞（HLMs）是肺中最丰富的免疫细胞，通过细胞因子和趋化因子的产生来发挥多种特殊功能。本项目旨在研究刺突蛋白对 HLMs 激活的影响，以及 ACE2 和 TMPRSS2 在 HLMs 中的表达。刺突蛋白诱导 HLMs 释放 CXCL8、IL-6、TNF-α 和 IL-1β；促进有效的吞噬作用；并通过增加 HLMs 溶酶体中的 Ca 含量来诱导细胞内 Ca 浓度的功能障碍。显微镜实验表明，HLMs 的追踪受到刺突蛋白激活的影响。最后，HLMs 组成性地表达 ACE2 和 TMPRSS2 的 mRNA。总之，在 SARS-CoV-2 感染期间，巨噬细胞似乎在肺损伤中发挥关键作用，导致免疫功能障碍和呼吸疾病。

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Function (Oxf). 2020 Jun 5;1(1):zqaa003. doi: 10.1093/function/zqaa003. eCollection 2020.
2
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Front Microbiol. 2022 Feb 10;13:789882. doi: 10.3389/fmicb.2022.789882. eCollection 2022.
3
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4
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Biomol Ther (Seoul). 2025 Mar 1;33(2):311-324. doi: 10.4062/biomolther.2025.004. Epub 2025 Feb 20.
5
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6
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