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屏息:自主神经对固有免疫的调节以抵御新冠病毒感染

Hold Breath: Autonomic Neural Regulation of Innate Immunity to Defend Against SARS-CoV-2 Infection.

作者信息

Wang Changle, Zhao Yan, Qiao Hongxiu, Gao Zhiyun, Yang Jing, Chuai Xia

机构信息

Department of Pathogenic Biology, Hebei Medical University, Shijiazhuang, China.

International Cooperation Laboratory of Stem Cell Research, Hebei Medical University, Shijiazhuang, China.

出版信息

Front Microbiol. 2022 Mar 3;12:819638. doi: 10.3389/fmicb.2021.819638. eCollection 2021.

DOI:10.3389/fmicb.2021.819638
PMID:35310398
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8929440/
Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel member of the genus of betacoronavirus, which caused a pandemic of coronavirus disease 2019 (COVID-19) worldwide. The innate immune system plays a critical role in eliminating the virus, which induces inflammatory cytokine and chemokine secretion, produces different interferons, and activates the adaptive immune system. Interactions between the autonomic nervous system and innate immunity release neurotransmitters or neuropeptides to balance the excess secretion of inflammatory cytokines, control the inflammation, and restore the host homeostasis. However, more neuro-immune mechanisms to defend against viral infection should be elucidated. Here, we mainly review and provide our understanding and viewpoint on the interaction between respiratory viral proteins and host cell receptors, innate immune responses to respiratory viral infection, and the autonomic neural regulation of the innate immune system to control respiratory viruses caused by lungs and airways inflammation.

摘要

严重急性呼吸综合征冠状病毒2(SARS-CoV-2)是β冠状病毒属的一个新成员,它在全球范围内引发了2019冠状病毒病(COVID-19)大流行。先天免疫系统在清除病毒过程中发挥着关键作用,该病毒会诱导炎性细胞因子和趋化因子的分泌,产生不同的干扰素,并激活适应性免疫系统。自主神经系统与先天免疫之间的相互作用会释放神经递质或神经肽,以平衡炎性细胞因子的过度分泌,控制炎症,并恢复宿主的内环境稳态。然而,更多抵御病毒感染的神经免疫机制仍有待阐明。在此,我们主要综述并阐述我们对呼吸道病毒蛋白与宿主细胞受体之间的相互作用、对呼吸道病毒感染的先天免疫反应以及先天免疫系统的自主神经调节以控制由肺部和气道炎症引起的呼吸道病毒的理解和观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5def/8929440/9a5443026069/fmicb-12-819638-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5def/8929440/9a5443026069/fmicb-12-819638-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5def/8929440/9a5443026069/fmicb-12-819638-g001.jpg

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