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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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| Published in: | Journal of cellular and molecular medicine 2019-02, Vol.23 (2), p.908-919 |
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| container_title | Journal of cellular and molecular medicine |
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| creator | 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 |
| description | 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 |
| doi_str_mv | 10.1111/jcmm.13992 |
| format | article |
| fullrecord | <record><control><sourceid>wiley_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6349191</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>JCMM13992</sourcerecordid><originalsourceid>FETCH-LOGICAL-p3442-10e16f22b1ea29e3870e67177887fe088bbd2552b65322f0c90acefcc92ab9d43</originalsourceid><addsrcrecordid>eNpVkUlOAzEQRS0EIiGw4QDIF0jw0IO9QYoiIEGJWDBsLdttB0fd7VYPoOw4AmfkJDgDEXjhKuk_f1X5A3CJ0QiHc73SRTHClHNyBPo4ZmQYcRod73vMKOuBs6ZZIUSTgJ2CHkU0ZSQmfeBm8-_PL5yOofZlWzvVtaaBrYfTp1cMXWmNbp0vA-PKrNMmg1IHBOZduQzyqqvXoUAJC981JtyZyaG3sOrywpcyqNap2jeuOQcnVuaNudjXAXi5u32eTIfzx_vZZDwfVjSKwrjI4MQSorCRhBvKUmSSFKcpY6k1iDGlMhLHRCUxJcQizZHUxmrNiVQ8i-gA3Ox8q04VJtMmrCVzUdWuCOMIL534r5TuTSz9u0hoxDHHweDqr8Hh5e-nBQDvgA-Xm_VBx0hs4hCbOMQ2DvEwWSy2Hf0B-HuBTA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>IL‐17A contributes to HSV1 infection‐induced acute lung injury in a mouse model of pulmonary fibrosis</title><source>Open Access: PubMed Central</source><source>Open Access: Wiley-Blackwell Open Access Journals</source><source>Publicly Available Content Database</source><creator>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</creator><creatorcontrib>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</creatorcontrib><description>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 < 0.0001), lower survival rate (100% vs 21.4%, P < 0.0001), poorer lung function and higher inflammatory response representing by increased total inflammatory cells in bronchoalveolar lavage fluid (BALF) (P = 0.0323), increased proportion of Th17 cells in peripheral blood (P = 0.0004) and higher inflammatory factors in BALF. In addition, HSV1 infection increased the expression of endoplasmic reticulum stress (ERS)‐related proteins in mice with BLM‐induced fibrosis. The inhibition of ERS by tauroursodeoxycholic acid (TUDCA, an ERS inhibitor) significantly reduced the IL‐17A levels in BALF (P = 0.0140) and TH17 cells in the peripheral blood (P = 0.0084) of mice with BLM+HSV1, suggesting that suppression of ERS may reduce TH17 response in mice with AE‐IPF. Compared with WT mice with BLM+HSV1, IL‐17A‐/‐ mice with BLM+HSV1 had lower ALI score (P = 0.0119), higher survival rate (78.6% vs 21.4%, P = 0.004), improved lung function, and milder inflammatory response.
Conclusions
HSV1 infection in addition to BLM‐induced IPF can successfully establish AE‐IPF in mice. IL‐17A and ERS promote lung inflammation in AE‐IPF development.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.13992</identifier><identifier>PMID: 30378252</identifier><language>eng</language><publisher>England: John Wiley and Sons Inc</publisher><subject>acute exacerbations of idiopathic pulmonary fibrosis ; Acute Lung Injury - chemically induced ; Acute Lung Injury - drug therapy ; Acute Lung Injury - mortality ; Acute Lung Injury - virology ; Animals ; Anti-Inflammatory Agents - pharmacology ; Antiviral Agents - pharmacology ; Bleomycin ; Bronchoalveolar Lavage Fluid - chemistry ; Bronchoalveolar Lavage Fluid - immunology ; Disease Models, Animal ; endoplasmic reticulum stress ; Endoplasmic Reticulum Stress - drug effects ; Endoplasmic Reticulum Stress - genetics ; Endoplasmic Reticulum Stress - immunology ; Gene Expression ; Herpes Simplex - chemically induced ; Herpes Simplex - drug therapy ; Herpes Simplex - mortality ; Herpes Simplex - virology ; herpes simplex virus 1 ; Herpesvirus 1, Human ; Humans ; Idiopathic Pulmonary Fibrosis - chemically induced ; Idiopathic Pulmonary Fibrosis - drug therapy ; Idiopathic Pulmonary Fibrosis - mortality ; Idiopathic Pulmonary Fibrosis - virology ; Interleukin-17 - deficiency ; Interleukin-17 - genetics ; Interleukin-17 - immunology ; interleukin‐17A ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Original ; Respiratory Function Tests ; Survival Analysis ; Taurochenodeoxycholic Acid - pharmacology ; Th17 Cells - drug effects ; Th17 Cells - immunology ; Th17 Cells - virology</subject><ispartof>Journal of cellular and molecular medicine, 2019-02, Vol.23 (2), p.908-919</ispartof><rights>2018 The Authors. published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0002-6998-9828</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6349191/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6349191/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,733,786,790,891,11589,27957,27958,46087,46511,53827,53829</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30378252$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Tao</creatorcontrib><creatorcontrib>Qiu, Hui</creatorcontrib><creatorcontrib>Zhao, Meng‐Meng</creatorcontrib><creatorcontrib>Chen, Shan‐Shan</creatorcontrib><creatorcontrib>Wu, Qin</creatorcontrib><creatorcontrib>Zhou, Nian‐Yu</creatorcontrib><creatorcontrib>Lu, Li‐Qin</creatorcontrib><creatorcontrib>Song, Jia‐Cui</creatorcontrib><creatorcontrib>Tang, Dan‐Li</creatorcontrib><creatorcontrib>Weng, Dong</creatorcontrib><creatorcontrib>Li, Hui‐Ping</creatorcontrib><title>IL‐17A contributes to HSV1 infection‐induced acute lung injury in a mouse model of pulmonary fibrosis</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>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 < 0.0001), lower survival rate (100% vs 21.4%, P < 0.0001), poorer lung function and higher inflammatory response representing by increased total inflammatory cells in bronchoalveolar lavage fluid (BALF) (P = 0.0323), increased proportion of Th17 cells in peripheral blood (P = 0.0004) and higher inflammatory factors in BALF. In addition, HSV1 infection increased the expression of endoplasmic reticulum stress (ERS)‐related proteins in mice with BLM‐induced fibrosis. The inhibition of ERS by tauroursodeoxycholic acid (TUDCA, an ERS inhibitor) significantly reduced the IL‐17A levels in BALF (P = 0.0140) and TH17 cells in the peripheral blood (P = 0.0084) of mice with BLM+HSV1, suggesting that suppression of ERS may reduce TH17 response in mice with AE‐IPF. Compared with WT mice with BLM+HSV1, IL‐17A‐/‐ mice with BLM+HSV1 had lower ALI score (P = 0.0119), higher survival rate (78.6% vs 21.4%, P = 0.004), improved lung function, and milder inflammatory response.
Conclusions
HSV1 infection in addition to BLM‐induced IPF can successfully establish AE‐IPF in mice. IL‐17A and ERS promote lung inflammation in AE‐IPF development.</description><subject>acute exacerbations of idiopathic pulmonary fibrosis</subject><subject>Acute Lung Injury - chemically induced</subject><subject>Acute Lung Injury - drug therapy</subject><subject>Acute Lung Injury - mortality</subject><subject>Acute Lung Injury - virology</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Antiviral Agents - pharmacology</subject><subject>Bleomycin</subject><subject>Bronchoalveolar Lavage Fluid - chemistry</subject><subject>Bronchoalveolar Lavage Fluid - immunology</subject><subject>Disease Models, Animal</subject><subject>endoplasmic reticulum stress</subject><subject>Endoplasmic Reticulum Stress - drug effects</subject><subject>Endoplasmic Reticulum Stress - genetics</subject><subject>Endoplasmic Reticulum Stress - immunology</subject><subject>Gene Expression</subject><subject>Herpes Simplex - chemically induced</subject><subject>Herpes Simplex - drug therapy</subject><subject>Herpes Simplex - mortality</subject><subject>Herpes Simplex - virology</subject><subject>herpes simplex virus 1</subject><subject>Herpesvirus 1, Human</subject><subject>Humans</subject><subject>Idiopathic Pulmonary Fibrosis - chemically induced</subject><subject>Idiopathic Pulmonary Fibrosis - drug therapy</subject><subject>Idiopathic Pulmonary Fibrosis - mortality</subject><subject>Idiopathic Pulmonary Fibrosis - virology</subject><subject>Interleukin-17 - deficiency</subject><subject>Interleukin-17 - genetics</subject><subject>Interleukin-17 - immunology</subject><subject>interleukin‐17A</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Original</subject><subject>Respiratory Function Tests</subject><subject>Survival Analysis</subject><subject>Taurochenodeoxycholic Acid - pharmacology</subject><subject>Th17 Cells - drug effects</subject><subject>Th17 Cells - immunology</subject><subject>Th17 Cells - virology</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><recordid>eNpVkUlOAzEQRS0EIiGw4QDIF0jw0IO9QYoiIEGJWDBsLdttB0fd7VYPoOw4AmfkJDgDEXjhKuk_f1X5A3CJ0QiHc73SRTHClHNyBPo4ZmQYcRod73vMKOuBs6ZZIUSTgJ2CHkU0ZSQmfeBm8-_PL5yOofZlWzvVtaaBrYfTp1cMXWmNbp0vA-PKrNMmg1IHBOZduQzyqqvXoUAJC981JtyZyaG3sOrywpcyqNap2jeuOQcnVuaNudjXAXi5u32eTIfzx_vZZDwfVjSKwrjI4MQSorCRhBvKUmSSFKcpY6k1iDGlMhLHRCUxJcQizZHUxmrNiVQ8i-gA3Ox8q04VJtMmrCVzUdWuCOMIL534r5TuTSz9u0hoxDHHweDqr8Hh5e-nBQDvgA-Xm_VBx0hs4hCbOMQ2DvEwWSy2Hf0B-HuBTA</recordid><startdate>201902</startdate><enddate>201902</enddate><creator>Chen, Tao</creator><creator>Qiu, Hui</creator><creator>Zhao, Meng‐Meng</creator><creator>Chen, Shan‐Shan</creator><creator>Wu, Qin</creator><creator>Zhou, Nian‐Yu</creator><creator>Lu, Li‐Qin</creator><creator>Song, Jia‐Cui</creator><creator>Tang, Dan‐Li</creator><creator>Weng, Dong</creator><creator>Li, Hui‐Ping</creator><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6998-9828</orcidid></search><sort><creationdate>201902</creationdate><title>IL‐17A contributes to HSV1 infection‐induced acute lung injury in a mouse model of pulmonary fibrosis</title><author>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</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p3442-10e16f22b1ea29e3870e67177887fe088bbd2552b65322f0c90acefcc92ab9d43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>acute exacerbations of idiopathic pulmonary fibrosis</topic><topic>Acute Lung Injury - chemically induced</topic><topic>Acute Lung Injury - drug therapy</topic><topic>Acute Lung Injury - mortality</topic><topic>Acute Lung Injury - virology</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Antiviral Agents - pharmacology</topic><topic>Bleomycin</topic><topic>Bronchoalveolar Lavage Fluid - chemistry</topic><topic>Bronchoalveolar Lavage Fluid - immunology</topic><topic>Disease Models, Animal</topic><topic>endoplasmic reticulum stress</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>Endoplasmic Reticulum Stress - genetics</topic><topic>Endoplasmic Reticulum Stress - immunology</topic><topic>Gene Expression</topic><topic>Herpes Simplex - chemically induced</topic><topic>Herpes Simplex - drug therapy</topic><topic>Herpes Simplex - mortality</topic><topic>Herpes Simplex - virology</topic><topic>herpes simplex virus 1</topic><topic>Herpesvirus 1, Human</topic><topic>Humans</topic><topic>Idiopathic Pulmonary Fibrosis - chemically induced</topic><topic>Idiopathic Pulmonary Fibrosis - drug therapy</topic><topic>Idiopathic Pulmonary Fibrosis - mortality</topic><topic>Idiopathic Pulmonary Fibrosis - virology</topic><topic>Interleukin-17 - deficiency</topic><topic>Interleukin-17 - genetics</topic><topic>Interleukin-17 - immunology</topic><topic>interleukin‐17A</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Original</topic><topic>Respiratory Function Tests</topic><topic>Survival Analysis</topic><topic>Taurochenodeoxycholic Acid - pharmacology</topic><topic>Th17 Cells - drug effects</topic><topic>Th17 Cells - immunology</topic><topic>Th17 Cells - virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Tao</creatorcontrib><creatorcontrib>Qiu, Hui</creatorcontrib><creatorcontrib>Zhao, Meng‐Meng</creatorcontrib><creatorcontrib>Chen, Shan‐Shan</creatorcontrib><creatorcontrib>Wu, Qin</creatorcontrib><creatorcontrib>Zhou, Nian‐Yu</creatorcontrib><creatorcontrib>Lu, Li‐Qin</creatorcontrib><creatorcontrib>Song, Jia‐Cui</creatorcontrib><creatorcontrib>Tang, Dan‐Li</creatorcontrib><creatorcontrib>Weng, Dong</creatorcontrib><creatorcontrib>Li, Hui‐Ping</creatorcontrib><collection>Open Access: Wiley-Blackwell Open Access Journals</collection><collection>Wiley Online Library</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Tao</au><au>Qiu, Hui</au><au>Zhao, Meng‐Meng</au><au>Chen, Shan‐Shan</au><au>Wu, Qin</au><au>Zhou, Nian‐Yu</au><au>Lu, Li‐Qin</au><au>Song, Jia‐Cui</au><au>Tang, Dan‐Li</au><au>Weng, Dong</au><au>Li, Hui‐Ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IL‐17A contributes to HSV1 infection‐induced acute lung injury in a mouse model of pulmonary fibrosis</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2019-02</date><risdate>2019</risdate><volume>23</volume><issue>2</issue><spage>908</spage><epage>919</epage><pages>908-919</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><notes>Tao Chen, Hui Qiu and Meng‐Meng Zhao contributed equally to this work.</notes><abstract>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 < 0.0001), lower survival rate (100% vs 21.4%, P < 0.0001), poorer lung function and higher inflammatory response representing by increased total inflammatory cells in bronchoalveolar lavage fluid (BALF) (P = 0.0323), increased proportion of Th17 cells in peripheral blood (P = 0.0004) and higher inflammatory factors in BALF. In addition, HSV1 infection increased the expression of endoplasmic reticulum stress (ERS)‐related proteins in mice with BLM‐induced fibrosis. The inhibition of ERS by tauroursodeoxycholic acid (TUDCA, an ERS inhibitor) significantly reduced the IL‐17A levels in BALF (P = 0.0140) and TH17 cells in the peripheral blood (P = 0.0084) of mice with BLM+HSV1, suggesting that suppression of ERS may reduce TH17 response in mice with AE‐IPF. Compared with WT mice with BLM+HSV1, IL‐17A‐/‐ mice with BLM+HSV1 had lower ALI score (P = 0.0119), higher survival rate (78.6% vs 21.4%, P = 0.004), improved lung function, and milder inflammatory response.
Conclusions
HSV1 infection in addition to BLM‐induced IPF can successfully establish AE‐IPF in mice. IL‐17A and ERS promote lung inflammation in AE‐IPF development.</abstract><cop>England</cop><pub>John Wiley and Sons Inc</pub><pmid>30378252</pmid><doi>10.1111/jcmm.13992</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-6998-9828</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of cellular and molecular medicine, 2019-02, Vol.23 (2), p.908-919 |
| issn | 1582-1838 1582-4934 |
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| source | Open Access: PubMed Central; Open Access: Wiley-Blackwell Open Access Journals; Publicly Available Content Database |
| subjects | acute exacerbations of idiopathic pulmonary fibrosis Acute Lung Injury - chemically induced Acute Lung Injury - drug therapy Acute Lung Injury - mortality Acute Lung Injury - virology Animals Anti-Inflammatory Agents - pharmacology Antiviral Agents - pharmacology Bleomycin Bronchoalveolar Lavage Fluid - chemistry Bronchoalveolar Lavage Fluid - immunology Disease Models, Animal endoplasmic reticulum stress Endoplasmic Reticulum Stress - drug effects Endoplasmic Reticulum Stress - genetics Endoplasmic Reticulum Stress - immunology Gene Expression Herpes Simplex - chemically induced Herpes Simplex - drug therapy Herpes Simplex - mortality Herpes Simplex - virology herpes simplex virus 1 Herpesvirus 1, Human Humans Idiopathic Pulmonary Fibrosis - chemically induced Idiopathic Pulmonary Fibrosis - drug therapy Idiopathic Pulmonary Fibrosis - mortality Idiopathic Pulmonary Fibrosis - virology Interleukin-17 - deficiency Interleukin-17 - genetics Interleukin-17 - immunology interleukin‐17A Male Mice Mice, Inbred C57BL Mice, Knockout Original Respiratory Function Tests Survival Analysis Taurochenodeoxycholic Acid - pharmacology Th17 Cells - drug effects Th17 Cells - immunology Th17 Cells - virology |
| title | IL‐17A contributes to HSV1 infection‐induced acute lung injury in a mouse model of pulmonary fibrosis |
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