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IL‐17A contributes to HSV1 infection‐induced acute lung injury in a mouse model of pulmonary fibrosis

Background Patients with idiopathic pulmonary fibrosis (IPF) often experience acute exacerbation (AE) after an episode of common cold. Aims To establish a mouse model of virus infection‐induced AE‐IPF and investigate the mechanism underlying the AE‐IPF. Methods Herpes simplex virus 1 (HSV1) was inoc...

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Bibliographic Details
Published in:Journal of cellular and molecular medicine 2019-02, Vol.23 (2), p.908-919
Main Authors: Chen, Tao, Qiu, Hui, Zhao, Meng‐Meng, Chen, Shan‐Shan, Wu, Qin, Zhou, Nian‐Yu, Lu, Li‐Qin, Song, Jia‐Cui, Tang, Dan‐Li, Weng, Dong, Li, Hui‐Ping
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Language:English
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Summary:Background Patients with idiopathic pulmonary fibrosis (IPF) often experience acute exacerbation (AE) after an episode of common cold. Aims To establish a mouse model of virus infection‐induced AE‐IPF and investigate the mechanism underlying the AE‐IPF. Methods Herpes simplex virus 1 (HSV1) was inoculated intranasally to wild‐type (WT) and IL‐17A gene knockout (IL‐17A‐/‐) mice 21 days after intratracheal administration of bleomycin (BLM). Results HSV1 infection caused acute exacerbation in mice with BLM‐induced fibrosis. Compared with the BLM+Saline mice, the mice with BLM+HSV1 showed significantly higher acute lung injury (ALI) score (P 
ISSN:1582-1838
1582-4934
DOI:10.1111/jcmm.13992