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COVID-19 时期的炎症小体

The Inflammasome in Times of COVID-19.

机构信息

DRV Ventures, LLC, Miami, FL, United States.

Department of Neurological Surgery and The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL, United States.

出版信息

Front Immunol. 2020 Oct 8;11:583373. doi: 10.3389/fimmu.2020.583373. eCollection 2020.


DOI:10.3389/fimmu.2020.583373
PMID:33149733
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7580384/
Abstract

Coronaviruses (CoVs) are members of the genus Betacoronavirus and the Coronaviridiae family responsible for infections such as severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and more recently, coronavirus disease-2019 (COVID-19). CoV infections present mainly as respiratory infections that lead to acute respiratory distress syndrome (ARDS). However, CoVs, such as COVID-19, also present as a hyperactivation of the inflammatory response that results in increased production of inflammatory cytokines such as interleukin (IL)-1β and its downstream molecule IL-6. The inflammasome is a multiprotein complex involved in the activation of caspase-1 that leads to the activation of IL-1β in a variety of diseases and infections such as CoV infection and in different tissues such as lungs, brain, intestines and kidneys, all of which have been shown to be affected in COVID-19 patients. Here we review the literature regarding the mechanism of inflammasome activation by CoV infection, the role of the inflammasome in ARDS, ventilator-induced lung injury (VILI), and Disseminated Intravascular Coagulation (DIC) as well as the potential mechanism by which the inflammasome may contribute to the damaging effects of inflammation in the cardiac, renal, digestive, and nervous systems in COVID-19 patients.

摘要

冠状病毒(CoV)属于β属冠状病毒和冠状病毒科,可引起严重急性呼吸综合征(SARS)、中东呼吸综合征(MERS)等疾病,最近还可引起 2019 年冠状病毒病(COVID-19)。CoV 感染主要表现为呼吸道感染,导致急性呼吸窘迫综合征(ARDS)。然而,CoV 如 COVID-19 也表现为炎症反应的过度激活,导致炎症细胞因子如白细胞介素(IL)-1β及其下游分子 IL-6 的产生增加。炎症小体是一种参与半胱天冬酶-1激活的多蛋白复合物,导致各种疾病和感染(如 CoV 感染)以及不同组织(如肺、脑、肠和肾)中 IL-1β的激活,所有这些组织都已被证明在 COVID-19 患者中受到影响。在这里,我们回顾了关于 CoV 感染引起炎症小体激活的机制、炎症小体在 ARDS、呼吸机诱导性肺损伤(VILI)和弥散性血管内凝血(DIC)中的作用,以及炎症小体可能在 COVID-19 患者的心脏、肾脏、消化系统和神经系统中炎症的破坏性作用中发挥作用的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d57d/7580384/94d96f008349/fimmu-11-583373-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d57d/7580384/6e78f6630e9f/fimmu-11-583373-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d57d/7580384/b44f6d1ea746/fimmu-11-583373-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d57d/7580384/67b97f2042ca/fimmu-11-583373-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d57d/7580384/94d96f008349/fimmu-11-583373-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d57d/7580384/6e78f6630e9f/fimmu-11-583373-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d57d/7580384/b44f6d1ea746/fimmu-11-583373-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d57d/7580384/67b97f2042ca/fimmu-11-583373-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d57d/7580384/94d96f008349/fimmu-11-583373-g0004.jpg

相似文献

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[2]
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[9]
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[4]
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[5]
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[6]
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[7]
Evaluation of the relationship between serum interleukin-1β levels and expression of inflammasome-related genes in patients with COVID-19.

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[8]
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[9]
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[10]
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本文引用的文献

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