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Article: Proinflammatory cytokine response and viral replication in mouse bone marrow derived macrophages infected with influenza H1N1 and H5N1 viruses

TitleProinflammatory cytokine response and viral replication in mouse bone marrow derived macrophages infected with influenza H1N1 and H5N1 viruses
Authors
Issue Date2012
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
PLoS One, 2012, v. 7 n. 11, p. e51057 How to Cite?
AbstractThe 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.
Persistent Identifierhttp://hdl.handle.net/10722/185606
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorChan, WY-
dc.contributor.authorLeung, CYH-
dc.contributor.authorNicholls, JM-
dc.contributor.authorPeiris, JSM-
dc.contributor.authorChan, MCW-
dc.date.accessioned2013-08-20T11:34:16Z-
dc.date.available2013-08-20T11:34:16Z-
dc.date.issued2012-
dc.identifier.citationPLoS One, 2012, v. 7 n. 11, p. e51057-
dc.identifier.issn1932-6203-
dc.identifier.urihttp://hdl.handle.net/10722/185606-
dc.description.abstractThe 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.-
dc.languageeng-
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action-
dc.relation.ispartofPLoS One-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleProinflammatory cytokine response and viral replication in mouse bone marrow derived macrophages infected with influenza H1N1 and H5N1 viruses-
dc.typeArticle-
dc.identifier.emailChan, WY: reneewy@hku.hk-
dc.identifier.emailLeung, CYH: cyhleung@hkucc.hku.hk-
dc.identifier.emailNicholls, JM: jmnichol@hkucc.hku.hk-
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hk-
dc.identifier.emailChan, MCW: mchan@hku.hk-
dc.identifier.authorityChan, WY=rp01596-
dc.identifier.authorityLeung, CYH=rp00307-
dc.identifier.authorityNicholls, JM=rp00364-
dc.identifier.authorityPeiris, JSM=rp00410-
dc.identifier.authorityChan, MCW=rp00420-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0051057-
dc.identifier.pmcidPMC3511392-
dc.identifier.hkuros216896-
dc.identifier.volume7-
dc.identifier.issue11-
dc.identifier.spagee51057-
dc.identifier.epagee51057-
dc.publisher.placeUnited States-

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