文章摘要

细胞因子风暴在2019新型冠状病毒肺炎肺损伤中的作用

作者: 1,2姜慧欣, 1,3黄学涵, 1,3林果, 1,4李志标, 1,3陈思豪, 5张润声, 6吴启文, 1涂永生
1 广州医科大学基础医学院生理学教研室，广州 511436
2 广州医科大学第二临床学院，广州 511436
3 广州医科大学第一临床学院，广州 511436
4 广州医科大学第三临床学院，广州 511436
5 广州市增城区人民医院消化内科，广州 511300
6 广州市增城区人民医院感染科，广州 511300
通讯: 涂永生 Email: tuys@gzhmu.edu.cn
DOI: 10.3978/j.issn.2095-6959.2022.02.031
基金: 广东省自然科学基金 (2018A0303130256)；广东省医学科研基金 (A2017315, A2018390,A2019042)；中国国家大学生创新创业培训计划 (202010570003)；中国国家大学生科技创新专项资金 (2018A028)；广东省大学生科技创新专项资金 (2018A009)；广东省科技创新战略专项资金 (pdjh2018b0419,pdjh2020b0486,pdjh2021b0411)；广州医科大学大学生实验室开放项目 (20181057000)；广州医科大学学生科技创新项目 (2017A006)。

摘要

2019新型冠状病毒肺炎(coronavirus disease 2019，COVID-19)是一种以肺为主要靶器官的全身多器官损伤性疾病。细胞因子风暴在COVID-19患者肺损伤中发挥重要作用，严重急性呼吸窘迫综合征冠状病毒-2靶向血管紧张素转换酶2(angiotensin-converting enzyme 2，ACE2)感染肺部的细胞，并引起以活化的巨噬细胞、中性粒细胞和T细胞为主的复杂免疫反应，这些细胞和受感染的细胞可在短时间内分泌大量的炎症因子，同时，炎症因子又可趋化更多的炎症细胞参与肺损伤过程，从而放大炎症效应造成肺的免疫损伤，此外，细胞因子风暴介导的其他器官损伤也可能对肺造成影响。本文总结了肺内细胞因子风暴的发生机制，并就炎症细胞[巨噬细胞(M1型与M2型巨噬细胞)、中性粒细胞和效应T细胞(辅助性T细胞17)]、细胞因子[白细胞介素(interleukin，IL)(IL-2，IL-17，IL-6，IL-1β)、肿瘤坏死因子(tumor necrosis factor，TNF) (TNF-α)、集落刺激因子(粒细胞集落刺激因子与粒细胞巨噬细胞集落刺激因子)]和趋化因子(干扰素-γ诱导蛋白10与巨噬细胞炎性蛋白1a)在COVID-19患者肺损伤的作用以及细胞因子风暴引发的肾衰竭和心脏损伤对肺的影响进行综述。
关键词： 2019新型冠状病毒肺炎；细胞因子风暴；肺损伤

Role of cytokine storm in lung injury of coronavirus disease 2019

Authors: 1,2JIANG Huixin, 1,3HUANG Xuehan, 1,3LIN Guo, 1,4LI Zhibiao, 1,3CHEN Sihao, 5ZHANG Runsheng, 6WU Qiwen, 1TU Yongsheng
1 Department of Physiology, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China
2 Second Clinical Medical College, Guangzhou Medical University, Guangzhou 511436, China
3 First Clinical Medical College, Guangzhou Medical University, Guangzhou 511436, China
4 Third Clinical Medical College, Guangzhou Medical University, Guangzhou 511436, China
5 Department of Gastroenterology, Zengcheng District People’s Hospital of Guangzhou, Guangzhou 511300, China
6 Department of Infectious Diseases, Zengcheng District People's Hospital of Guangzhou, Guangzhou 511300, China

CorrespondingAuthor: TU Yongsheng Email: tuys@gzhmu.edu.cn

DOI: 10.3978/j.issn.2095-6959.2022.02.031

Foundation: This work was supported by the Natural Science Foundations of Guangdong Province (2018A0303130256), the Medical Scienti c Research Foundation of Guangdong Province (A2017315, A2018390, and A2019042), the National College Students’ Innovation Entrepreneurship Training Program of China (202010570003), Special Funds for the Scienti c and Technological Innovation of National College Students of China (2018A028), Special Funds for the Scienti c and Technological Innovation of Guangdong Provincial College Students (2018A009), Special Funds for the Strategy of Guangdong Provincial Scienti c and Technological Innovation, and “Climbing Program” Special Funds (pdjh2018b0419, pdjh2020b0486, and pdjh2021b0411), the Laboratory Open Project for College Students of Guangzhou Medical University (20181057000), and the Guangzhou Medical University College Students Science Technology Innovation Project (2017A006), China.

Abstract

Coronavirus disease 2019 (COVID-19) is a systemic multi-organ injury disease with the lung as the main target organ. Cytokine storm plays an important role in lung injury in patients with COVID-19. Severe acute respiratory syndrome coronavirus-2 enters target cells via interaction with angiotensin-converting enzyme 2 (ACE2) receptor, thus triggering a complex immune response characterized by activation of macrophages, neutrophils, and T cells. These cells and infected cells release several types of inflammatory cytokines in a short time, drawing more inflammatory cells to the infected tissue to participate in the damage process, which amplifies the effects of inflammation causing immune damage to the lung. Furthermore, other organs damage mediated by the cytokine storm could affect the lung. Therefore, this paper summarizes the mechanisms of cytokine storm in lung and reviews the effects of inflammatory cells [macrophages (M1-type macrophages and M2-type macrophages), neutrophils and effector T cells (T helper cell 17)], cytokines [interleukins (IL) (IL-2, IL-17, IL-6, IL-1β), tumor necrosis factor (TNF) (TNF-α), colony stimulating factor (granulocyte colony stimulating factor and granulocyte-macrophage colony stimulating factor)] and chemokines (interferon-inducible protein 10 and macrophage inflammatory protein-1a) on lung injury in COVID-19 patients, and the effects of cytokine storm-induced renal failure and heart injury on lung.
Keywords： coronavirus disease 2019 (COVID-19); cytokine storm; lung injury

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