Proinflammatory cytokine response and viral replication in mouse bone marrow derived macrophages infected with influenza H1N1 and H5N1 viruses
The pathogenesis of human influenza H5N1 virus infection remains poorly understood and controversial. Cytokine dysregulation in human infection has been hypothesized to contribute to disease severity. We developed in vitro cultures of mouse bone marrow derived macrophages (BMDMΦ) from C57BL/6N mouse...
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| description | The pathogenesis of human influenza H5N1 virus infection remains poorly understood and controversial. Cytokine dysregulation in human infection has been hypothesized to contribute to disease severity. We developed in vitro cultures of mouse bone marrow derived macrophages (BMDMΦ) from C57BL/6N mouse to compare influenza A (H5N1 and H1N1) virus replication and pro-inflammatory cytokine and chemokine responses. While both H1N1 and H5N1 viruses infected the mouse bone marrow derived macrophages, only the H1N1 virus had showed evidence of productive viral replication from the infected cells. In comparison with human seasonal influenza H1N1 (A/HK/54/98) and mouse adapted influenza H1N1 (A/WSN/33) viruses, the highly pathogenic influenza H5N1 virus (A/HK/483/97) was a more potent inducer of the chemokine, CXCL 10 (IP-10), while there was not a clear differential TNF-α protein expression pattern. Although human influenza viruses rarely cause infection in mice without prior adaption, the use of in vitro cell cultures of primary mouse cells is of interest, especially given the availability of gene-defective (knock-out) mice for specific genes. |
| doi_str_mv | 10.1371/journal.pone.0051057 |
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Cytokine dysregulation in human infection has been hypothesized to contribute to disease severity. We developed in vitro cultures of mouse bone marrow derived macrophages (BMDMΦ) from C57BL/6N mouse to compare influenza A (H5N1 and H1N1) virus replication and pro-inflammatory cytokine and chemokine responses. While both H1N1 and H5N1 viruses infected the mouse bone marrow derived macrophages, only the H1N1 virus had showed evidence of productive viral replication from the infected cells. In comparison with human seasonal influenza H1N1 (A/HK/54/98) and mouse adapted influenza H1N1 (A/WSN/33) viruses, the highly pathogenic influenza H5N1 virus (A/HK/483/97) was a more potent inducer of the chemokine, CXCL 10 (IP-10), while there was not a clear differential TNF-α protein expression pattern. Although human influenza viruses rarely cause infection in mice without prior adaption, the use of in vitro cell cultures of primary mouse cells is of interest, especially given the availability of gene-defective (knock-out) mice for specific genes.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0051057</identifier><identifier>PMID: 23226456</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animals ; Avian influenza ; Avian influenza viruses ; Biology ; Bone marrow ; Chemokines - genetics ; Chemokines - metabolism ; Cytokines ; Cytokines - genetics ; Cytokines - metabolism ; Cytokines - secretion ; Female ; Fluorescent Antibody Technique ; Gene Expression Regulation ; Health aspects ; Humans ; Infection ; Infections ; Inflammation ; Inflammation Mediators - metabolism ; Influenza ; Influenza A ; Influenza A Virus, H1N1 Subtype - physiology ; Influenza A Virus, H5N1 Subtype - physiology ; Influenza, Human - virology ; IP-10 protein ; Lectins - metabolism ; Macrophages ; Macrophages - immunology ; Macrophages - pathology ; Macrophages - secretion ; Macrophages - virology ; Medicine ; Mice ; Mice, Inbred C57BL ; Orthomyxoviridae Infections - immunology ; Orthomyxoviridae Infections - pathology ; Orthomyxoviridae Infections - virology ; Pandemics ; Pathogenesis ; Replication ; Studies ; Swine flu ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Viral Load ; Viral Matrix Proteins - genetics ; Viral Matrix Proteins - metabolism ; Virus replication ; Virus Replication - physiology ; Viruses</subject><ispartof>PloS one, 2012-11, Vol.7 (11), p.e51057-e51057</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Chan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2012 Chan et al 2012 Chan et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-e716c403ca0463d99dd4d7df0a5f2afa6686663998c183a2057c45daf2c8c5313</citedby><cites>FETCH-LOGICAL-c692t-e716c403ca0463d99dd4d7df0a5f2afa6686663998c183a2057c45daf2c8c5313</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3511392/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3511392/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23226456$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Chamaillard, Mathias</contributor><creatorcontrib>Chan, Renee W Y</creatorcontrib><creatorcontrib>Leung, Connie Y H</creatorcontrib><creatorcontrib>Nicholls, John M</creatorcontrib><creatorcontrib>Peiris, J S Malik</creatorcontrib><creatorcontrib>Chan, Michael C W</creatorcontrib><title>Proinflammatory cytokine response and viral replication in mouse bone marrow derived macrophages infected with influenza H1N1 and H5N1 viruses</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The pathogenesis of human influenza H5N1 virus infection remains poorly understood and controversial. Cytokine dysregulation in human infection has been hypothesized to contribute to disease severity. We developed in vitro cultures of mouse bone marrow derived macrophages (BMDMΦ) from C57BL/6N mouse to compare influenza A (H5N1 and H1N1) virus replication and pro-inflammatory cytokine and chemokine responses. While both H1N1 and H5N1 viruses infected the mouse bone marrow derived macrophages, only the H1N1 virus had showed evidence of productive viral replication from the infected cells. In comparison with human seasonal influenza H1N1 (A/HK/54/98) and mouse adapted influenza H1N1 (A/WSN/33) viruses, the highly pathogenic influenza H5N1 virus (A/HK/483/97) was a more potent inducer of the chemokine, CXCL 10 (IP-10), while there was not a clear differential TNF-α protein expression pattern. Although human influenza viruses rarely cause infection in mice without prior adaption, the use of in vitro cell cultures of primary mouse cells is of interest, especially given the availability of gene-defective (knock-out) mice for specific genes.</description><subject>Analysis</subject><subject>Animals</subject><subject>Avian influenza</subject><subject>Avian influenza viruses</subject><subject>Biology</subject><subject>Bone marrow</subject><subject>Chemokines - genetics</subject><subject>Chemokines - metabolism</subject><subject>Cytokines</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Cytokines - secretion</subject><subject>Female</subject><subject>Fluorescent Antibody Technique</subject><subject>Gene Expression Regulation</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Infection</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Inflammation Mediators - metabolism</subject><subject>Influenza</subject><subject>Influenza A</subject><subject>Influenza A Virus, H1N1 Subtype - physiology</subject><subject>Influenza A Virus, H5N1 Subtype - physiology</subject><subject>Influenza, Human - virology</subject><subject>IP-10 protein</subject><subject>Lectins - metabolism</subject><subject>Macrophages</subject><subject>Macrophages - immunology</subject><subject>Macrophages - pathology</subject><subject>Macrophages - secretion</subject><subject>Macrophages - virology</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Orthomyxoviridae Infections - immunology</subject><subject>Orthomyxoviridae Infections - pathology</subject><subject>Orthomyxoviridae Infections - virology</subject><subject>Pandemics</subject><subject>Pathogenesis</subject><subject>Replication</subject><subject>Studies</subject><subject>Swine flu</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Viral Load</subject><subject>Viral Matrix Proteins - genetics</subject><subject>Viral Matrix Proteins - metabolism</subject><subject>Virus replication</subject><subject>Virus Replication - physiology</subject><subject>Viruses</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk82O0zAQxyMEYpeFN0AQCQnBocUfiZNckFYroJVWLOLrak1sp3VJ4mInXcpD8MxM2uyqRXtAOcQe_-Y_nhlPFD2lZEp5Rt-sXO9bqKdr15opISklaXYvOqUFZxPBCL9_sD6JHoWwQojnQjyMThhnTCSpOI3-fPLOtlUNTQOd89tYbTv3w7Ym9iagdDAxtDreWA81mta1VdBZ18a2jRvX43GJ8eMGvHfXsTbebozGrfJuvYSFCQhWRnVovLbdctjVvWl_QzyjH-lOe5biAgOgWHgcPaigDubJ-D-Lvr1_9_ViNrm8-jC_OL-cKFGwbmIyKlRCuAKSCK6LQutEZ7oikFYMKhAC8xS8KHJFcw4MS6OSVEPFVK5STvlZ9Hyvu65dkGMpg6R8KCMnCUdivie0g5Vce4spbqUDK3cG5xcSfGdVbSQrRFXqKi8Lw5KSJTmkCtIyIRlPNVEMtd6O0fqyMVqZtsNyHoken7R2KRduI_E6lBeDwKtRwLufvQmdbGxQpq6hNdgESRnPEBUkR_TFP-jd2Y3UAjABbIrDuGoQledJJoqCix01vYPCT5vGKux7ZdF-5PD6yAGZzvzqFtCHIOdfPv8_e_X9mH15wC4N1N0yuLofXmI4BpM9iO8vBG-q2yJTIoexuamGHMZGjmODbs8OG3TrdDMn_C_e3RQl</recordid><startdate>20121130</startdate><enddate>20121130</enddate><creator>Chan, Renee W Y</creator><creator>Leung, Connie Y H</creator><creator>Nicholls, John M</creator><creator>Peiris, J S Malik</creator><creator>Chan, Michael C W</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</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>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20121130</creationdate><title>Proinflammatory cytokine response and viral replication in mouse bone marrow derived macrophages infected with influenza H1N1 and H5N1 viruses</title><author>Chan, Renee W Y ; Leung, Connie Y H ; Nicholls, John M ; Peiris, J S Malik ; Chan, Michael C W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-e716c403ca0463d99dd4d7df0a5f2afa6686663998c183a2057c45daf2c8c5313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Avian influenza</topic><topic>Avian influenza viruses</topic><topic>Biology</topic><topic>Bone marrow</topic><topic>Chemokines - 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Cytokine dysregulation in human infection has been hypothesized to contribute to disease severity. We developed in vitro cultures of mouse bone marrow derived macrophages (BMDMΦ) from C57BL/6N mouse to compare influenza A (H5N1 and H1N1) virus replication and pro-inflammatory cytokine and chemokine responses. While both H1N1 and H5N1 viruses infected the mouse bone marrow derived macrophages, only the H1N1 virus had showed evidence of productive viral replication from the infected cells. In comparison with human seasonal influenza H1N1 (A/HK/54/98) and mouse adapted influenza H1N1 (A/WSN/33) viruses, the highly pathogenic influenza H5N1 virus (A/HK/483/97) was a more potent inducer of the chemokine, CXCL 10 (IP-10), while there was not a clear differential TNF-α protein expression pattern. Although human influenza viruses rarely cause infection in mice without prior adaption, the use of in vitro cell cultures of primary mouse cells is of interest, especially given the availability of gene-defective (knock-out) mice for specific genes.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23226456</pmid><doi>10.1371/journal.pone.0051057</doi><tpages>e51057</tpages><oa>free_for_read</oa></addata></record> |
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| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Analysis Animals Avian influenza Avian influenza viruses Biology Bone marrow Chemokines - genetics Chemokines - metabolism Cytokines Cytokines - genetics Cytokines - metabolism Cytokines - secretion Female Fluorescent Antibody Technique Gene Expression Regulation Health aspects Humans Infection Infections Inflammation Inflammation Mediators - metabolism Influenza Influenza A Influenza A Virus, H1N1 Subtype - physiology Influenza A Virus, H5N1 Subtype - physiology Influenza, Human - virology IP-10 protein Lectins - metabolism Macrophages Macrophages - immunology Macrophages - pathology Macrophages - secretion Macrophages - virology Medicine Mice Mice, Inbred C57BL Orthomyxoviridae Infections - immunology Orthomyxoviridae Infections - pathology Orthomyxoviridae Infections - virology Pandemics Pathogenesis Replication Studies Swine flu Tumor necrosis factor-TNF Tumor necrosis factor-α Viral Load Viral Matrix Proteins - genetics Viral Matrix Proteins - metabolism Virus replication Virus Replication - physiology Viruses |
| title | Proinflammatory cytokine response and viral replication in mouse bone marrow derived macrophages infected with influenza H1N1 and H5N1 viruses |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-30T13%3A55%3A29IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Proinflammatory%20cytokine%20response%20and%20viral%20replication%20in%20mouse%20bone%20marrow%20derived%20macrophages%20infected%20with%20influenza%20H1N1%20and%20H5N1%20viruses&rft.jtitle=PloS%20one&rft.au=Chan,%20Renee%20W%20Y&rft.date=2012-11-30&rft.volume=7&rft.issue=11&rft.spage=e51057&rft.epage=e51057&rft.pages=e51057-e51057&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0051057&rft_dat=%3Cgale_plos_%3EA476993643%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1351053043&rft_id=info:pmid/23226456&rft_galeid=A476993643&rft_doaj_id=oai_doaj_org_article_296fbdf8b9e24b248a5ca5b40735d0c2&rfr_iscdi=true |