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Compared with the BLM<\/jats:styled-content>+Saline mice, the mice with BLM<\/jats:styled-content>+HSV<\/jats:styled-content>1 showed significantly higher acute lung injury (ALI<\/jats:styled-content>) score (P\u00a0<\/jats:italic><\u00a0<\/jats:italic>0.0001), lower survival rate (100% vs 21.4%, P\u00a0<\u00a0<\/jats:italic>0.0001), poorer lung function and higher inflammatory response representing by increased total inflammatory cells in bronchoalveolar lavage fluid (BALF<\/jats:styled-content>) (P\u00a0<\/jats:italic>=\u00a0<\/jats:italic>0.0323), increased proportion of Th17 cells in peripheral blood (P\u00a0<\/jats:italic>=\u00a0<\/jats:italic>0.0004) and higher inflammatory factors in BALF<\/jats:styled-content>. In addition, HSV<\/jats:styled-content>1 infection increased the expression of endoplasmic reticulum stress (ERS<\/jats:styled-content>)\u2010related proteins in mice with BLM<\/jats:styled-content>\u2010induced fibrosis. The inhibition of ERS<\/jats:styled-content> by tauroursodeoxycholic acid (TUDCA<\/jats:styled-content>, an ERS<\/jats:styled-content> inhibitor) significantly reduced the IL<\/jats:styled-content>\u201017A levels in BALF<\/jats:styled-content> (P\u00a0<\/jats:italic>=\u00a0<\/jats:italic>0.0140) and TH<\/jats:styled-content>17 cells in the peripheral blood (P\u00a0<\/jats:italic>=\u00a0<\/jats:italic>0.0084) of mice with BLM<\/jats:styled-content>+HSV<\/jats:styled-content>1, suggesting that suppression of ERS<\/jats:styled-content> may reduce TH<\/jats:styled-content>17 response in mice with AE<\/jats:styled-content>\u2010IPF<\/jats:styled-content>. Compared with WT<\/jats:styled-content> mice with BLM<\/jats:styled-content>+HSV<\/jats:styled-content>1, IL<\/jats:styled-content>\u201017A\u2010\/\u2010<\/jats:sup> mice with BLM<\/jats:styled-content>+HSV<\/jats:styled-content>1 had lower ALI<\/jats:styled-content> score (P\u00a0<\/jats:italic>=\u00a0<\/jats:italic>0.0119), higher survival rate (78.6% vs 21.4%, P\u00a0<\/jats:italic>=\u00a0<\/jats:italic>0.004), improved lung function, and milder inflammatory response.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>HSV<\/jats:styled-content>1 infection in addition to BLM<\/jats:styled-content>\u2010induced IPF<\/jats:styled-content> can successfully establish AE<\/jats:styled-content>\u2010IPF<\/jats:styled-content> in mice. IL<\/jats:styled-content>\u201017A and ERS<\/jats:styled-content> promote lung inflammation in AE<\/jats:styled-content>\u2010IPF<\/jats:styled-content> development.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jcmm.13992","type":"journal-article","created":{"date-parts":[[2018,10,31]],"date-time":"2018-10-31T05:20:55Z","timestamp":1540963255000},"page":"908-919","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["IL<\/scp>\u201017A contributes to HSV<\/scp>1 infection\u2010induced acute lung injury in a mouse model of pulmonary fibrosis"],"prefix":"10.1111","volume":"23","author":[{"given":"Tao","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Respiratory Medicine School of Medicine Shanghai Pulmonary Hospital Tongji University Shanghai China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hui","family":"Qiu","sequence":"additional","affiliation":[{"name":"Department of Respiratory 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