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COVID-19 发病机制中的促炎细胞因子:出了什么问题?

The pro-inflammatory cytokines in COVID-19 pathogenesis: What goes wrong?

机构信息

Molecular Genetics and Immunophysiopathology Research Team, Health and Environment Laboratory, Aïn Chock Faculty of Sciences, Hassan II University of Casablanca (UH2C), Morocco.

Immunopathology of Infectious and Systemic Diseases, Laboratory of Cellular and Molecular Pathology, Faculty of Medicine and Pharmacy, UH2C, Morocco.

出版信息

Microb Pathog. 2021 Apr;153:104799. doi: 10.1016/j.micpath.2021.104799. Epub 2021 Feb 18.

DOI:10.1016/j.micpath.2021.104799
PMID:33609650
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7889464/
Abstract

The outbreak of coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection, has emerged in China in December 2019 and rapidly spread to more than 196 countries worldwide. The physiopathology of human SARS-CoV-2 has not been completely understood, but its pathogenesis has been linked to a disproportionate response of the immune system. Just as described for SARS and MERS, an uncontrolled systemic inflammatory response, known as cytokine release syndrome (CRS) was observed in severe COVID-19 patients. It results from the release by immune and non-immune effector cells of substantial amounts of pro-inflammatory cytokines and appears to contribute to SARS-CoV-2 pulmonary inflammation and extensive lung damage. In addition, hyper-coagulation and thrombosis resulted from the important release of pro-inflammatory cytokines contribute to the lethality of subjects severely infected with SARS-CoV-2. It is therefore essential to have a deep understanding of the various cytokines involved in this exacerbated immune response, and that could be targeted by potential immunological treatments. The aim of this review was to gather the current knowledge about the role of pro-inflammatory cytokines, namely IL-1β, IL-6, IL-8, IL-17 and TNFα in SARS-CoV-2 CRS, the probable causes and clinical outcomes of this phenomenon in severe cases of COVID-19.

摘要

2019 年冠状病毒病(COVID-19)的爆发是由严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)感染引起的,于 2019 年 12 月在中国出现,并迅速传播到全球 196 多个国家。人类 SARS-CoV-2 的病理生理学尚未完全了解,但已将其发病机制与免疫系统的过度反应联系起来。正如 SARS 和 MERS 所描述的那样,在严重的 COVID-19 患者中观察到了一种称为细胞因子释放综合征(CRS)的不受控制的全身炎症反应。它是由免疫和非免疫效应细胞大量释放促炎细胞因子引起的,似乎导致 SARS-CoV-2 肺部炎症和广泛的肺损伤。此外,由于促炎细胞因子的大量释放导致的高凝和血栓形成导致 SARS-CoV-2 严重感染的患者死亡率较高。因此,深入了解参与这种加剧免疫反应的各种细胞因子至关重要,这些细胞因子可能是潜在免疫治疗的靶点。本综述的目的是汇集目前关于促炎细胞因子(即 IL-1β、IL-6、IL-8、IL-17 和 TNFα)在 SARS-CoV-2 CRS 中的作用、COVID-19 严重病例中这种现象的可能原因和临床结果的知识。

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