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SARS-CoV-2 刺突蛋白抑制猴肺支气管肺泡灌洗液原代细胞中的 ACE2 和 I 型干扰素表达。

SARS-CoV-2 Spike Protein Suppresses ACE2 and Type I Interferon Expression in Primary Cells From Macaque Lung Bronchoalveolar Lavage.

机构信息

Vaccine Branch, Center of Cancer Research, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD, United States.

Biostatistics and Data Management Section, Center of Cancer Research, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD, United States.

出版信息

Front Immunol. 2021 Jun 4;12:658428. doi: 10.3389/fimmu.2021.658428. eCollection 2021.

DOI:10.3389/fimmu.2021.658428
PMID:34149696
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8213020/
Abstract

SARS-CoV-2 virus causes upper and lower respiratory diseases including pneumonia, and in some cases, leads to lethal pulmonary failure. Angiotensin converting enzyme-2 (ACE2), the receptor for cellular entry of SARS-CoV-2 virus, has been shown to protect against severe acute lung failure. Here, we provide evidence that SARS-CoV-2 spike protein S1 reduced the mRNA expression of ACE2 and type I interferons in primary cells of lung bronchoalveolar lavage (BAL) from naïve rhesus macaques. The expression levels of ACE2 and type I interferons were also found to be correlated with each other, consistent with the recent finding that ACE2 is an interferon-inducible gene. Furthermore, induction of ACE2 and type I interferons by poly I:C, an interferon inducer, was suppressed by S1 protein in primary cells of BAL. These observations suggest that the downregulation of ACE2 and type I interferons induced by S1 protein may directly contribute to SARS-CoV-2-associated lung diseases.

摘要

严重急性呼吸综合征冠状病毒 2 型（SARS-CoV-2）病毒可引起上呼吸道和下呼吸道疾病，包括肺炎，在某些情况下，还可导致致命性的肺衰竭。血管紧张素转换酶 2（ACE2）是 SARS-CoV-2 病毒进入细胞的受体，已被证明可预防严重急性肺衰竭。在这里，我们提供的证据表明，SARS-CoV-2 刺突蛋白 S1 降低了来自天真恒河猴肺支气管肺泡灌洗液（BAL）的原代细胞中 ACE2 和 I 型干扰素的 mRNA 表达。ACE2 和 I 型干扰素的表达水平也相互关联，这与 ACE2 是干扰素诱导基因的最近发现一致。此外，干扰素诱导剂 poly I:C 诱导的 ACE2 和 I 型干扰素在 BAL 的原代细胞中被 S1 蛋白抑制。这些观察结果表明，S1 蛋白诱导的 ACE2 和 I 型干扰素下调可能直接导致与 SARS-CoV-2 相关的肺部疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c838/8213020/6dbfcc77af57/fimmu-12-658428-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c838/8213020/4bf61d6a984e/fimmu-12-658428-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c838/8213020/97bf5efaaace/fimmu-12-658428-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c838/8213020/2e932fe73f3f/fimmu-12-658428-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c838/8213020/12afe2b9f49c/fimmu-12-658428-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c838/8213020/6dbfcc77af57/fimmu-12-658428-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c838/8213020/4bf61d6a984e/fimmu-12-658428-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c838/8213020/97bf5efaaace/fimmu-12-658428-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c838/8213020/2e932fe73f3f/fimmu-12-658428-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c838/8213020/12afe2b9f49c/fimmu-12-658428-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c838/8213020/6dbfcc77af57/fimmu-12-658428-g005.jpg

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本文引用的文献

[1]
Protection against SARS-CoV-2 infection by a mucosal vaccine in rhesus macaques.

JCI Insight. 2021-4-28

[2]
COVID-19, Angiotensin-Converting Enzyme 2 and Renin-Angiotensin System Inhibition: Implications for Practice.

Curr Hypertens Rev. 2022

[3]
Friend or foe? ACE2 inhibitors and GLP-1R agonists in COVID-19 treatment.

Obes Med. 2021-3

[4]
ACE2 Interaction Networks in COVID-19: A Physiological Framework for Prediction of Outcome in Patients with Cardiovascular Risk Factors.

J Clin Med. 2020-11-21

[5]
Interferons and viruses induce a novel truncated ACE2 isoform and not the full-length SARS-CoV-2 receptor.

Nat Genet. 2020-10-19

[6]
Autoantibodies against type I IFNs in patients with life-threatening COVID-19.

Science. 2020-9-24

[7]
Inborn errors of type I IFN immunity in patients with life-threatening COVID-19.

Science. 2020-9-24

[8]
A Prime/Boost Vaccine Regimen Alters the Rectal Microbiome and Impacts Immune Responses and Viremia Control Post-Simian Immunodeficiency Virus Infection in Male and Female Rhesus Macaques.

J Virol. 2020-11-23

[9]
Type I Interferon Susceptibility Distinguishes SARS-CoV-2 from SARS-CoV.

J Virol. 2020-11-9

[10]
Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients.

Science. 2020-7-13

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