Infection with influenza virus induces IL-33 in murine lungs
IL-33, a novel IL-1 family member, is crucially expressed and involved in pulmonary diseases, but its regulation in viral diseases such as influenza A virus (IAV) remains unclear. This study aimed to characterize the expression and release of IL-33 in lungs of IAV-infected mice in vivo and in murine...
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| Veröffentlicht in: | American journal of respiratory cell and molecular biology 2011-12, Vol.45 (6), p.1125-1132 |
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| creator | Le Goffic, Ronan Arshad, Muhammad Imran Rauch, Michel L'Helgoualc'h, Annie Delmas, Bernard Piquet-Pellorce, Claire Samson, Michel |
| description | IL-33, a novel IL-1 family member, is crucially expressed and involved in pulmonary diseases, but its regulation in viral diseases such as influenza A virus (IAV) remains unclear. This study aimed to characterize the expression and release of IL-33 in lungs of IAV-infected mice in vivo and in murine respiratory epithelial cells (MLE-15) in vitro. Our results provide evidence of up-regulation of IL-33 mRNA in IAV-infected murine lungs, compared with noninfected control mice. The overexpression of IL-33 was positively correlated with a significant increase in mRNA encoding the proinflammatory cytokines TNF-α, IFN-γ, IL-1β, and IL-6, and was also associated with an increase in IFN-β mRNA. A profound overexpression of IL-33 protein was evident in IAV-infected murine lungs and bronchoalveolar lavages of influenza-infected mice, compared with low concentrations in naive lungs in vivo. Immunolocalization highlighted the cellular expression of IL-33 in alveolar epithelial and endothelial cells, along with increased infiltrate cells in virus-infected lungs. Further in vitro experiments showed an induction of IL-33 transcript-in MLE-15 cells and human epithelial cells (A549) infected with different strains of IAV in comparison with noninfected cells. In conclusion, our findings evidenced a profound expression of IL-33 in lungs during both in vivo and in vitro IAV infections, suggesting a role for IL-33 in virus-induced lung infections. |
| doi_str_mv | 10.1165/rcmb.2010-0516OC |
| format | Article |
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This study aimed to characterize the expression and release of IL-33 in lungs of IAV-infected mice in vivo and in murine respiratory epithelial cells (MLE-15) in vitro. Our results provide evidence of up-regulation of IL-33 mRNA in IAV-infected murine lungs, compared with noninfected control mice. The overexpression of IL-33 was positively correlated with a significant increase in mRNA encoding the proinflammatory cytokines TNF-α, IFN-γ, IL-1β, and IL-6, and was also associated with an increase in IFN-β mRNA. A profound overexpression of IL-33 protein was evident in IAV-infected murine lungs and bronchoalveolar lavages of influenza-infected mice, compared with low concentrations in naive lungs in vivo. Immunolocalization highlighted the cellular expression of IL-33 in alveolar epithelial and endothelial cells, along with increased infiltrate cells in virus-infected lungs. Further in vitro experiments showed an induction of IL-33 transcript-in MLE-15 cells and human epithelial cells (A549) infected with different strains of IAV in comparison with noninfected cells. In conclusion, our findings evidenced a profound expression of IL-33 in lungs during both in vivo and in vitro IAV infections, suggesting a role for IL-33 in virus-induced lung infections.</description><identifier>ISSN: 1044-1549</identifier><identifier>EISSN: 1535-4989</identifier><identifier>DOI: 10.1165/rcmb.2010-0516OC</identifier><identifier>PMID: 21642589</identifier><language>eng</language><publisher>United States: American Thoracic Society</publisher><subject>Animals ; Bronchoalveolar Lavage ; Cell Line ; Endothelial Cells ; Endothelial Cells - immunology ; Endothelial Cells - metabolism ; Endothelial Cells - virology ; Epithelial Cells ; Epithelial Cells - immunology ; Epithelial Cells - metabolism ; Epithelial Cells - virology ; Female ; Gene Expression Regulation ; Gene Expression Regulation - immunology ; Human health and pathology ; Humans ; Influenza A Virus, H1N1 Subtype ; Influenza A Virus, H1N1 Subtype - immunology ; Influenza A Virus, H1N1 Subtype - metabolism ; Influenza A Virus, H3N2 Subtype ; Influenza A Virus, H3N2 Subtype - immunology ; Influenza A Virus, H3N2 Subtype - metabolism ; Interferon-beta ; Interferon-beta - biosynthesis ; Interferon-beta - immunology ; Interferon-gamma ; Interferon-gamma - biosynthesis ; Interferon-gamma - immunology ; Interleukin-1beta ; Interleukin-1beta - biosynthesis ; Interleukin-1beta - immunology ; Interleukin-33 ; Interleukin-6 ; Interleukin-6 - biosynthesis ; Interleukin-6 - immunology ; Interleukins ; Interleukins - biosynthesis ; Interleukins - immunology ; Life Sciences ; Lung ; Lung - immunology ; Lung - metabolism ; Lung - virology ; Mice ; Orthomyxoviridae Infections ; Orthomyxoviridae Infections - immunology ; Orthomyxoviridae Infections - metabolism ; RNA, Messenger ; RNA, Messenger - biosynthesis ; RNA, Messenger - immunology ; Tumor Necrosis Factor-alpha ; Tumor Necrosis Factor-alpha - biosynthesis ; Tumor Necrosis Factor-alpha - immunology</subject><ispartof>American journal of respiratory cell and molecular biology, 2011-12, Vol.45 (6), p.1125-1132</ispartof><rights>Copyright American Thoracic Society Dec 2011</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c401t-e98bc3cd90ea312cb4ff4d315fe99a7f7190d69ce1a4ec912547c187767761763</citedby><cites>FETCH-LOGICAL-c401t-e98bc3cd90ea312cb4ff4d315fe99a7f7190d69ce1a4ec912547c187767761763</cites><orcidid>0000-0002-2012-0064</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21642589$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00681982$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Le Goffic, Ronan</creatorcontrib><creatorcontrib>Arshad, Muhammad Imran</creatorcontrib><creatorcontrib>Rauch, Michel</creatorcontrib><creatorcontrib>L'Helgoualc'h, Annie</creatorcontrib><creatorcontrib>Delmas, Bernard</creatorcontrib><creatorcontrib>Piquet-Pellorce, Claire</creatorcontrib><creatorcontrib>Samson, Michel</creatorcontrib><title>Infection with influenza virus induces IL-33 in murine lungs</title><title>American journal of respiratory cell and molecular biology</title><addtitle>Am J Respir Cell Mol Biol</addtitle><description>IL-33, a novel IL-1 family member, is crucially expressed and involved in pulmonary diseases, but its regulation in viral diseases such as influenza A virus (IAV) remains unclear. This study aimed to characterize the expression and release of IL-33 in lungs of IAV-infected mice in vivo and in murine respiratory epithelial cells (MLE-15) in vitro. Our results provide evidence of up-regulation of IL-33 mRNA in IAV-infected murine lungs, compared with noninfected control mice. The overexpression of IL-33 was positively correlated with a significant increase in mRNA encoding the proinflammatory cytokines TNF-α, IFN-γ, IL-1β, and IL-6, and was also associated with an increase in IFN-β mRNA. A profound overexpression of IL-33 protein was evident in IAV-infected murine lungs and bronchoalveolar lavages of influenza-infected mice, compared with low concentrations in naive lungs in vivo. Immunolocalization highlighted the cellular expression of IL-33 in alveolar epithelial and endothelial cells, along with increased infiltrate cells in virus-infected lungs. Further in vitro experiments showed an induction of IL-33 transcript-in MLE-15 cells and human epithelial cells (A549) infected with different strains of IAV in comparison with noninfected cells. In conclusion, our findings evidenced a profound expression of IL-33 in lungs during both in vivo and in vitro IAV infections, suggesting a role for IL-33 in virus-induced lung infections.</description><subject>Animals</subject><subject>Bronchoalveolar Lavage</subject><subject>Cell Line</subject><subject>Endothelial Cells</subject><subject>Endothelial Cells - immunology</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - virology</subject><subject>Epithelial Cells</subject><subject>Epithelial Cells - immunology</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - virology</subject><subject>Female</subject><subject>Gene Expression Regulation</subject><subject>Gene Expression Regulation - immunology</subject><subject>Human health and pathology</subject><subject>Humans</subject><subject>Influenza A Virus, H1N1 Subtype</subject><subject>Influenza A Virus, H1N1 Subtype - immunology</subject><subject>Influenza A Virus, H1N1 Subtype - 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virology</subject><subject>Mice</subject><subject>Orthomyxoviridae Infections</subject><subject>Orthomyxoviridae Infections - immunology</subject><subject>Orthomyxoviridae Infections - metabolism</subject><subject>RNA, Messenger</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - immunology</subject><subject>Tumor Necrosis Factor-alpha</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><issn>1044-1549</issn><issn>1535-4989</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkc9LwzAUx4MoTqd3T1K8iIfOvDZpE_AyhrpBYRc9hzRNXUd_zKSZ6F9vSucOQiD5hs_7Pt77InQDeAaQ0EejmnwWYcAhppCsFyfoAmhMQ8IZP_VvTEgIlPAJurR2izFEDOAcTSJISEQZv0BPq7bUqq-6Nviq-k1QtWXtdPsjg31lnPW6cErbYJWFcexV0DhTtTqoXfthr9BZKWurrw_3FL2_PL8tlmG2fl0t5lmoCIY-1JzlKlYFx1rGEKmclCUpYqCl5lymZQocFwlXGiTRikNESaqApWniD6RJPEUPo-9G1mJnqkaab9HJSiznmRj-ME4YcBbtwbP3I7sz3afTthdNZZWua9nqzlnBMUv97DT15N0_cts50_pBBAcgjEMy2OERUqaz1ujy2B-wGDIQQwZiyECMGfiS24OvyxtdHAv-lh7_Ap1qf_A</recordid><startdate>201112</startdate><enddate>201112</enddate><creator>Le Goffic, Ronan</creator><creator>Arshad, Muhammad Imran</creator><creator>Rauch, Michel</creator><creator>L'Helgoualc'h, Annie</creator><creator>Delmas, Bernard</creator><creator>Piquet-Pellorce, Claire</creator><creator>Samson, Michel</creator><general>American Thoracic Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><orcidid>https://orcid.org/0000-0002-2012-0064</orcidid></search><sort><creationdate>201112</creationdate><title>Infection with influenza virus induces IL-33 in murine lungs</title><author>Le Goffic, Ronan ; Arshad, Muhammad Imran ; Rauch, Michel ; L'Helgoualc'h, Annie ; Delmas, Bernard ; Piquet-Pellorce, Claire ; Samson, Michel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c401t-e98bc3cd90ea312cb4ff4d315fe99a7f7190d69ce1a4ec912547c187767761763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Bronchoalveolar Lavage</topic><topic>Cell Line</topic><topic>Endothelial Cells</topic><topic>Endothelial Cells - 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Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><jtitle>American journal of respiratory cell and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Le Goffic, Ronan</au><au>Arshad, Muhammad Imran</au><au>Rauch, Michel</au><au>L'Helgoualc'h, Annie</au><au>Delmas, Bernard</au><au>Piquet-Pellorce, Claire</au><au>Samson, Michel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Infection with influenza virus induces IL-33 in murine lungs</atitle><jtitle>American journal of respiratory cell and molecular biology</jtitle><addtitle>Am J Respir Cell Mol Biol</addtitle><date>2011-12</date><risdate>2011</risdate><volume>45</volume><issue>6</issue><spage>1125</spage><epage>1132</epage><pages>1125-1132</pages><issn>1044-1549</issn><eissn>1535-4989</eissn><abstract>IL-33, a novel IL-1 family member, is crucially expressed and involved in pulmonary diseases, but its regulation in viral diseases such as influenza A virus (IAV) remains unclear. This study aimed to characterize the expression and release of IL-33 in lungs of IAV-infected mice in vivo and in murine respiratory epithelial cells (MLE-15) in vitro. Our results provide evidence of up-regulation of IL-33 mRNA in IAV-infected murine lungs, compared with noninfected control mice. The overexpression of IL-33 was positively correlated with a significant increase in mRNA encoding the proinflammatory cytokines TNF-α, IFN-γ, IL-1β, and IL-6, and was also associated with an increase in IFN-β mRNA. A profound overexpression of IL-33 protein was evident in IAV-infected murine lungs and bronchoalveolar lavages of influenza-infected mice, compared with low concentrations in naive lungs in vivo. Immunolocalization highlighted the cellular expression of IL-33 in alveolar epithelial and endothelial cells, along with increased infiltrate cells in virus-infected lungs. Further in vitro experiments showed an induction of IL-33 transcript-in MLE-15 cells and human epithelial cells (A549) infected with different strains of IAV in comparison with noninfected cells. In conclusion, our findings evidenced a profound expression of IL-33 in lungs during both in vivo and in vitro IAV infections, suggesting a role for IL-33 in virus-induced lung infections.</abstract><cop>United States</cop><pub>American Thoracic Society</pub><pmid>21642589</pmid><doi>10.1165/rcmb.2010-0516OC</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-2012-0064</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | American journal of respiratory cell and molecular biology, 2011-12, Vol.45 (6), p.1125-1132 |
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| subjects | Animals Bronchoalveolar Lavage Cell Line Endothelial Cells Endothelial Cells - immunology Endothelial Cells - metabolism Endothelial Cells - virology Epithelial Cells Epithelial Cells - immunology Epithelial Cells - metabolism Epithelial Cells - virology Female Gene Expression Regulation Gene Expression Regulation - immunology Human health and pathology Humans Influenza A Virus, H1N1 Subtype Influenza A Virus, H1N1 Subtype - immunology Influenza A Virus, H1N1 Subtype - metabolism Influenza A Virus, H3N2 Subtype Influenza A Virus, H3N2 Subtype - immunology Influenza A Virus, H3N2 Subtype - metabolism Interferon-beta Interferon-beta - biosynthesis Interferon-beta - immunology Interferon-gamma Interferon-gamma - biosynthesis Interferon-gamma - immunology Interleukin-1beta Interleukin-1beta - biosynthesis Interleukin-1beta - immunology Interleukin-33 Interleukin-6 Interleukin-6 - biosynthesis Interleukin-6 - immunology Interleukins Interleukins - biosynthesis Interleukins - immunology Life Sciences Lung Lung - immunology Lung - metabolism Lung - virology Mice Orthomyxoviridae Infections Orthomyxoviridae Infections - immunology Orthomyxoviridae Infections - metabolism RNA, Messenger RNA, Messenger - biosynthesis RNA, Messenger - immunology Tumor Necrosis Factor-alpha Tumor Necrosis Factor-alpha - biosynthesis Tumor Necrosis Factor-alpha - immunology |
| title | Infection with influenza virus induces IL-33 in murine lungs |
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