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病毒感染与哮喘气道上皮免疫

Viral Infection and Airway Epithelial Immunity in Asthma.

机构信息

Division of Respiratory Medicine and Allergy, Department of Internal Medicine, Medical School of Jeonbuk National University, 20 Geonji-ro, Deokjin-gu, Jeonju 54907, Korea.

出版信息

Int J Mol Sci. 2022 Aug 31;23(17):9914. doi: 10.3390/ijms23179914.

DOI:10.3390/ijms23179914
PMID:36077310
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9456547/
Abstract

Viral respiratory tract infections are associated with asthma development and exacerbation in children and adults. In the course of immune responses to viruses, airway epithelial cells are the initial platform of innate immunity against viral invasion. Patients with severe asthma are more vulnerable than those with mild to moderate asthma to viral infections. Furthermore, in most cases, asthmatic patients tend to produce lower levels of antiviral cytokines than healthy subjects, such as interferons produced from immune effector cells and airway epithelial cells. The epithelial inflammasome appears to contribute to asthma exacerbation through overactivation, leading to self-damage, despite its naturally protective role against infectious pathogens. Given the mixed and complex immune responses in viral-infection-induced asthma exacerbation, this review examines the diverse roles of airway epithelial immunity and related potential therapeutic targets and discusses the mechanisms underlying the heterogeneous manifestations of asthma exacerbations.

摘要

病毒性呼吸道感染与儿童和成人的哮喘发病和加重有关。在对病毒的免疫反应过程中,气道上皮细胞是固有免疫抵抗病毒入侵的初始平台。重症哮喘患者比轻至中度哮喘患者更容易受到病毒感染。此外,在大多数情况下,哮喘患者产生的抗病毒细胞因子水平低于健康受试者,例如免疫效应细胞和气道上皮细胞产生的干扰素。尽管上皮细胞炎性小体在对抗感染性病原体方面具有天然的保护作用,但它的过度激活似乎导致了哮喘加重的自身损伤。鉴于病毒感染引起的哮喘加重中的混合和复杂免疫反应,本综述检查了气道上皮免疫的不同作用及其相关的潜在治疗靶点,并讨论了哮喘加重表现异质性的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66bd/9456547/d9a180723158/ijms-23-09914-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66bd/9456547/c4e73265fdab/ijms-23-09914-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66bd/9456547/ea8eb79dbd5a/ijms-23-09914-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66bd/9456547/d9a180723158/ijms-23-09914-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66bd/9456547/c4e73265fdab/ijms-23-09914-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66bd/9456547/ea8eb79dbd5a/ijms-23-09914-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66bd/9456547/d9a180723158/ijms-23-09914-g003.jpg

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