Effect of IL-6 deficiency on susceptibility to HSV-1 respiratory infection and intrinsic macrophage antiviral resistance
Cytokines play important roles in the mechanisms of disease development. Interleukin-6 (IL-6) is associated with clearance of herpes simplex virus (HSV) infections and in virus-induced immunopathology. However, the importance of IL-6 in host defense against HSV-1 respiratory infection is unknown. Th...
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| Veröffentlicht in: | Journal of interferon & cytokine research 2008-10, Vol.28 (10), p.589-596 |
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| creator | Murphy, E Angela Davis, J Mark Brown, Adrienne S Carmichael, Martin D Ghaffar, Abdul Mayer, Eugene P |
| description | Cytokines play important roles in the mechanisms of disease development. Interleukin-6 (IL-6) is associated with clearance of herpes simplex virus (HSV) infections and in virus-induced immunopathology. However, the importance of IL-6 in host defense against HSV-1 respiratory infection is unknown. This study tested the effect of knockout mice deficient for IL-6 on susceptibility to HSV-1 respiratory infection and on intrinsic macrophage antiviral resistance to HSV-1. Control C57BL/6 IL-6+/+ mice and IL-6 knockout mice (IL-6-/-) were intranasally inoculated with 50 microL of a standardized dose (3.2 x 10(5)) of HSV-1. Morbidity, mortality, and symptom severity were monitored for 21 days. A subset of mice was sacrificed at 48-h postinfection and lungs were analyzed for viral titers. Peritoneal macrophages were obtained from a third set of mice and assayed for antiviral resistance to HSV-1. IL-6-/- increased morbidity by 84%, mortality by 84%, and symptom severity score on days 7.5 through 11 (p < 0.05). IL-6-/- increased virus titers in the lung 4-fold (p < 0.01) and resulted in a decrease in macrophage antiviral resistance (p < 0.001). Results indicate that IL-6 plays an important role in susceptibility to respiratory infection in mice, which may be mediated at least in part by its effect on macrophage antiviral resistance. |
| doi_str_mv | 10.1089/jir.2007.0103 |
| format | Article |
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Interleukin-6 (IL-6) is associated with clearance of herpes simplex virus (HSV) infections and in virus-induced immunopathology. However, the importance of IL-6 in host defense against HSV-1 respiratory infection is unknown. This study tested the effect of knockout mice deficient for IL-6 on susceptibility to HSV-1 respiratory infection and on intrinsic macrophage antiviral resistance to HSV-1. Control C57BL/6 IL-6+/+ mice and IL-6 knockout mice (IL-6-/-) were intranasally inoculated with 50 microL of a standardized dose (3.2 x 10(5)) of HSV-1. Morbidity, mortality, and symptom severity were monitored for 21 days. A subset of mice was sacrificed at 48-h postinfection and lungs were analyzed for viral titers. Peritoneal macrophages were obtained from a third set of mice and assayed for antiviral resistance to HSV-1. IL-6-/- increased morbidity by 84%, mortality by 84%, and symptom severity score on days 7.5 through 11 (p < 0.05). IL-6-/- increased virus titers in the lung 4-fold (p < 0.01) and resulted in a decrease in macrophage antiviral resistance (p < 0.001). Results indicate that IL-6 plays an important role in susceptibility to respiratory infection in mice, which may be mediated at least in part by its effect on macrophage antiviral resistance.</description><identifier>ISSN: 1079-9907</identifier><identifier>EISSN: 1557-7465</identifier><identifier>DOI: 10.1089/jir.2007.0103</identifier><identifier>PMID: 18778200</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Animals ; Disease susceptibility ; Disease Susceptibility - immunology ; Health aspects ; Herpes ; Herpes Simplex - immunology ; Herpes Simplex - mortality ; Herpes Simplex - virology ; Herpes simplex virus 1 ; Herpesvirus 1, Human - immunology ; Herpesvirus diseases ; Interleukin-6 ; Interleukin-6 - deficiency ; Interleukin-6 - immunology ; Macrophages ; Macrophages - immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Risk factors ; Viral Load</subject><ispartof>Journal of interferon & cytokine research, 2008-10, Vol.28 (10), p.589-596</ispartof><rights>COPYRIGHT 2008 Mary Ann Liebert, Inc.</rights><rights>(©) © Mary Ann Liebert, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-4464272ffcb2b817435cbb05888c1ac82b64cb4f7a5a9d99c267a27120dc057d3</citedby><cites>FETCH-LOGICAL-c482t-4464272ffcb2b817435cbb05888c1ac82b64cb4f7a5a9d99c267a27120dc057d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18778200$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Murphy, E Angela</creatorcontrib><creatorcontrib>Davis, J Mark</creatorcontrib><creatorcontrib>Brown, Adrienne S</creatorcontrib><creatorcontrib>Carmichael, Martin D</creatorcontrib><creatorcontrib>Ghaffar, Abdul</creatorcontrib><creatorcontrib>Mayer, Eugene P</creatorcontrib><title>Effect of IL-6 deficiency on susceptibility to HSV-1 respiratory infection and intrinsic macrophage antiviral resistance</title><title>Journal of interferon & cytokine research</title><addtitle>J Interferon Cytokine Res</addtitle><description>Cytokines play important roles in the mechanisms of disease development. Interleukin-6 (IL-6) is associated with clearance of herpes simplex virus (HSV) infections and in virus-induced immunopathology. However, the importance of IL-6 in host defense against HSV-1 respiratory infection is unknown. This study tested the effect of knockout mice deficient for IL-6 on susceptibility to HSV-1 respiratory infection and on intrinsic macrophage antiviral resistance to HSV-1. Control C57BL/6 IL-6+/+ mice and IL-6 knockout mice (IL-6-/-) were intranasally inoculated with 50 microL of a standardized dose (3.2 x 10(5)) of HSV-1. Morbidity, mortality, and symptom severity were monitored for 21 days. A subset of mice was sacrificed at 48-h postinfection and lungs were analyzed for viral titers. Peritoneal macrophages were obtained from a third set of mice and assayed for antiviral resistance to HSV-1. IL-6-/- increased morbidity by 84%, mortality by 84%, and symptom severity score on days 7.5 through 11 (p < 0.05). IL-6-/- increased virus titers in the lung 4-fold (p < 0.01) and resulted in a decrease in macrophage antiviral resistance (p < 0.001). Results indicate that IL-6 plays an important role in susceptibility to respiratory infection in mice, which may be mediated at least in part by its effect on macrophage antiviral resistance.</description><subject>Animals</subject><subject>Disease susceptibility</subject><subject>Disease Susceptibility - immunology</subject><subject>Health aspects</subject><subject>Herpes</subject><subject>Herpes Simplex - immunology</subject><subject>Herpes Simplex - mortality</subject><subject>Herpes Simplex - virology</subject><subject>Herpes simplex virus 1</subject><subject>Herpesvirus 1, Human - immunology</subject><subject>Herpesvirus diseases</subject><subject>Interleukin-6</subject><subject>Interleukin-6 - deficiency</subject><subject>Interleukin-6 - immunology</subject><subject>Macrophages</subject><subject>Macrophages - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Risk factors</subject><subject>Viral Load</subject><issn>1079-9907</issn><issn>1557-7465</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFks1rFDEYxoMotlaPXiUoeJttks1MkmMp1RYWPFi9hkwmqVlmkjHJiPvf9x12QZSC5JCv3_Py5smD0FtKNpRIdbkPecMIERtCyfYZOqdtKxrBu_Y5rIlQjVJEnKFXpewJIZ1k6iU6o1IICapz9PvGe2crTh7f7ZoOD84HG1y0B5wiLkuxbq6hD2OoB1wTvv36vaE4uzKHbGrKBxziWiAAbeIAu5pDLMHiydic5h_mwcFFDb-AH1dhKNVE616jF96Mxb05zRfo26eb--vbZvfl89311a6xXLLacN5xJpj3tme9pIJvW9v3pJVSWmqsZH3Hbc-9MK1Rg1KWdcIwQRkZLGnFsL1AH49155x-Lq5UPQV41Dia6NJSdKc60ioq_gtSMJJATwC-_wfcpyVHeIRm4D5nikmAPhyhBzM6DR6lmo1dK-orcL_tGJBAbZ6gYAxuCjZF-Aw4_0vQHAXgbSnZeT3nMJl80JToNQ8a8qDXPOg1D8C_O_W69JMb_tCnAGwfARpSr5A</recordid><startdate>200810</startdate><enddate>200810</enddate><creator>Murphy, E Angela</creator><creator>Davis, J Mark</creator><creator>Brown, Adrienne S</creator><creator>Carmichael, Martin D</creator><creator>Ghaffar, Abdul</creator><creator>Mayer, Eugene P</creator><general>Mary Ann Liebert, Inc</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>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8C1</scope><scope>8FD</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>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>200810</creationdate><title>Effect of IL-6 deficiency on susceptibility to HSV-1 respiratory infection and intrinsic macrophage antiviral resistance</title><author>Murphy, E Angela ; Davis, J Mark ; Brown, Adrienne S ; Carmichael, Martin D ; Ghaffar, Abdul ; Mayer, Eugene P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-4464272ffcb2b817435cbb05888c1ac82b64cb4f7a5a9d99c267a27120dc057d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Disease susceptibility</topic><topic>Disease Susceptibility - immunology</topic><topic>Health aspects</topic><topic>Herpes</topic><topic>Herpes Simplex - immunology</topic><topic>Herpes Simplex - mortality</topic><topic>Herpes Simplex - virology</topic><topic>Herpes simplex virus 1</topic><topic>Herpesvirus 1, Human - immunology</topic><topic>Herpesvirus diseases</topic><topic>Interleukin-6</topic><topic>Interleukin-6 - deficiency</topic><topic>Interleukin-6 - immunology</topic><topic>Macrophages</topic><topic>Macrophages - immunology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Risk factors</topic><topic>Viral Load</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Murphy, E Angela</creatorcontrib><creatorcontrib>Davis, J Mark</creatorcontrib><creatorcontrib>Brown, Adrienne S</creatorcontrib><creatorcontrib>Carmichael, Martin D</creatorcontrib><creatorcontrib>Ghaffar, Abdul</creatorcontrib><creatorcontrib>Mayer, Eugene P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of interferon & cytokine research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Murphy, E Angela</au><au>Davis, J Mark</au><au>Brown, Adrienne S</au><au>Carmichael, Martin D</au><au>Ghaffar, Abdul</au><au>Mayer, Eugene P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of IL-6 deficiency on susceptibility to HSV-1 respiratory infection and intrinsic macrophage antiviral resistance</atitle><jtitle>Journal of interferon & cytokine research</jtitle><addtitle>J Interferon Cytokine Res</addtitle><date>2008-10</date><risdate>2008</risdate><volume>28</volume><issue>10</issue><spage>589</spage><epage>596</epage><pages>589-596</pages><issn>1079-9907</issn><eissn>1557-7465</eissn><abstract>Cytokines play important roles in the mechanisms of disease development. Interleukin-6 (IL-6) is associated with clearance of herpes simplex virus (HSV) infections and in virus-induced immunopathology. However, the importance of IL-6 in host defense against HSV-1 respiratory infection is unknown. This study tested the effect of knockout mice deficient for IL-6 on susceptibility to HSV-1 respiratory infection and on intrinsic macrophage antiviral resistance to HSV-1. Control C57BL/6 IL-6+/+ mice and IL-6 knockout mice (IL-6-/-) were intranasally inoculated with 50 microL of a standardized dose (3.2 x 10(5)) of HSV-1. Morbidity, mortality, and symptom severity were monitored for 21 days. A subset of mice was sacrificed at 48-h postinfection and lungs were analyzed for viral titers. Peritoneal macrophages were obtained from a third set of mice and assayed for antiviral resistance to HSV-1. IL-6-/- increased morbidity by 84%, mortality by 84%, and symptom severity score on days 7.5 through 11 (p < 0.05). IL-6-/- increased virus titers in the lung 4-fold (p < 0.01) and resulted in a decrease in macrophage antiviral resistance (p < 0.001). Results indicate that IL-6 plays an important role in susceptibility to respiratory infection in mice, which may be mediated at least in part by its effect on macrophage antiviral resistance.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>18778200</pmid><doi>10.1089/jir.2007.0103</doi><tpages>8</tpages></addata></record> |
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| ispartof | Journal of interferon & cytokine research, 2008-10, Vol.28 (10), p.589-596 |
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| subjects | Animals Disease susceptibility Disease Susceptibility - immunology Health aspects Herpes Herpes Simplex - immunology Herpes Simplex - mortality Herpes Simplex - virology Herpes simplex virus 1 Herpesvirus 1, Human - immunology Herpesvirus diseases Interleukin-6 Interleukin-6 - deficiency Interleukin-6 - immunology Macrophages Macrophages - immunology Mice Mice, Inbred C57BL Mice, Knockout Risk factors Viral Load |
| title | Effect of IL-6 deficiency on susceptibility to HSV-1 respiratory infection and intrinsic macrophage antiviral resistance |
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