Author:
Long Xin,Xie Jun,Ren Luo,Yu Guangyuan,Liu Enmei,Deng Yu,Long Xiaoru
Abstract
Abstract
Background
IL-17A is a pleiotropic cytokine and intimately associated with asthma, but its role in respiratory syncytial virus (RSV) infection is conflicting in the literature.
Methods
Children hospitalized in the respiratory department with RSV infection during RSV pandemic season of 2018–2020 were included. Nasopharyngeal aspirates were collected for pathogen and cytokines determination. In the murine model, RSV intranasal administrations were performed in wild-type and IL-17A-/- mice. Leukocytes and cytokines in bronchoalveolar lavage fluid (BALF), lung histopathology, and airway hyperresponsiveness (AHR) were measured. RORγt mRNA and IL-23R mRNA were semi-quantified by qPCR.
Results
IL-17A increased significantly in RSV-infected children and was positively associated with pneumonia severity. In the murine model, IL-17A significantly increased in BALF of mice with RSV infection. Airway inflammation, lung tissue damage and AHR were significantly alleviated in wild-type mice following IL-17A neutralization and in the IL-17A-/- mice. IL-17A decreased by removing CD4+ T cells but increased by depleting CD8+ T cells. IL-6, IL-21, RORγt mRNA and IL-23R mRNA dramatically increased in parallel with the rise of IL-17A.
Conclusions
IL-17A contributes to the airway dysfunctions induced by RSV in children and murine. CD3+CD4+T cells are its major cellular sources and the IL-6/IL-21-IL-23R-RORγt signaling pathway might participate in its regulation.
Funder
National Natural Science Foundation of China
Natural Science Foundation of Chongqing, China
Returned Overseas Students Entrepreneurship Innovation Support Program
Newton international fellowship
Scientific and Technological Research Program of Chongqing Municipal Education Commission
Chongqing Science and Health Joint Medical Research Project
Publisher
Springer Science and Business Media LLC
Subject
Infectious Diseases,Virology
Cited by
1 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献