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Article: Cytokine profiles induced by the novel swine-origin influenza A/H1N1 virus: Implications for treatment strategies

TitleCytokine profiles induced by the novel swine-origin influenza A/H1N1 virus: Implications for treatment strategies
Authors
Issue Date2010
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
Citation
Journal Of Infectious Diseases, 2010, v. 201 n. 3, p. 346-353 How to Cite?
AbstractBackground. Given the apparent high mortality associated with the novel swine-origin influenza A/H1N1 virus (S-OIV) in Mexico, we aimed to study the cytokine profiles induced by S-OIV and the effect of immunomodulators. Methods. We assayed cytokines and their messenger RNA (mRNA) levels in culture supernatants of human macrophages infected with H5N1, S-OIV California/04/2009 (S-OIV-CA), S-OIV Hong Kong/415742 (S-OIV-HK), or seasonal H1N1 with or without celecoxib and mesalazine. Results. Among the 12 cytokines showing detectable levels, levels of 8 proinflammatory cytokines (interleukin [IL] 2R, IL-6, interferon [IFN] α, macrophage inflammatory protein [MIP] α, MIP-1β, IFN-induced protein 10, regulated on activation, normal T cell expressed and secreted [RANTES], and monocyte chemotactic protein [MCP] 1) were higher in cells infected by H5N1 but similar among cells infected with H1N1, S-OIV-CA, or S-OIV-HK. The levels of the other 4 cytokines were similar for H5N1, H1N1, S-OIV-CA and S-OIV-HK. Among the 8 cytokines induced by H5N1, 6 were suppressed by celecoxib and mesalazine. The mRNA levels of tumor necrosis factor α, IFN-γ, IL-6, and MCP-1 induced by H5N1 were higher than the levels of other cytokines at 12 and/or 24 h. Conclusions. No major cytokine storm, as seen in H5N1 infection, is associated with S-OIV infection of cell lines. The mainstay of treatment for uncomplicated S-OIV infections should be antiviral agents without immunomodulators. For individual S-OIV-infected patients with severe primary viral pneumonia, severe sepsis, and multiorgan failure, immunomodulators may be considered as an adjunctive therapy in clinical trials. © 2009 by the Infectious Diseases Society of America. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/157577
ISSN
2015 Impact Factor: 6.344
2015 SCImago Journal Rankings: 4.000
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWoo, PCYen_US
dc.contributor.authorTung, ETKen_US
dc.contributor.authorChan, KHen_US
dc.contributor.authorLau, CCYen_US
dc.contributor.authorLau, SKPen_US
dc.contributor.authorYuen, KYen_US
dc.date.accessioned2012-08-08T08:51:24Z-
dc.date.available2012-08-08T08:51:24Z-
dc.date.issued2010en_US
dc.identifier.citationJournal Of Infectious Diseases, 2010, v. 201 n. 3, p. 346-353en_US
dc.identifier.issn0022-1899en_US
dc.identifier.urihttp://hdl.handle.net/10722/157577-
dc.description.abstractBackground. Given the apparent high mortality associated with the novel swine-origin influenza A/H1N1 virus (S-OIV) in Mexico, we aimed to study the cytokine profiles induced by S-OIV and the effect of immunomodulators. Methods. We assayed cytokines and their messenger RNA (mRNA) levels in culture supernatants of human macrophages infected with H5N1, S-OIV California/04/2009 (S-OIV-CA), S-OIV Hong Kong/415742 (S-OIV-HK), or seasonal H1N1 with or without celecoxib and mesalazine. Results. Among the 12 cytokines showing detectable levels, levels of 8 proinflammatory cytokines (interleukin [IL] 2R, IL-6, interferon [IFN] α, macrophage inflammatory protein [MIP] α, MIP-1β, IFN-induced protein 10, regulated on activation, normal T cell expressed and secreted [RANTES], and monocyte chemotactic protein [MCP] 1) were higher in cells infected by H5N1 but similar among cells infected with H1N1, S-OIV-CA, or S-OIV-HK. The levels of the other 4 cytokines were similar for H5N1, H1N1, S-OIV-CA and S-OIV-HK. Among the 8 cytokines induced by H5N1, 6 were suppressed by celecoxib and mesalazine. The mRNA levels of tumor necrosis factor α, IFN-γ, IL-6, and MCP-1 induced by H5N1 were higher than the levels of other cytokines at 12 and/or 24 h. Conclusions. No major cytokine storm, as seen in H5N1 infection, is associated with S-OIV infection of cell lines. The mainstay of treatment for uncomplicated S-OIV infections should be antiviral agents without immunomodulators. For individual S-OIV-infected patients with severe primary viral pneumonia, severe sepsis, and multiorgan failure, immunomodulators may be considered as an adjunctive therapy in clinical trials. © 2009 by the Infectious Diseases Society of America. All rights reserved.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.orgen_US
dc.relation.ispartofJournal of Infectious Diseasesen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCytokines - Genetics - Metabolismen_US
dc.subject.meshDogsen_US
dc.subject.meshEpithelial Cells - Metabolismen_US
dc.subject.meshGene Expression Regulation - Immunologyen_US
dc.subject.meshHumansen_US
dc.subject.meshInfluenza A Virus, H1n1 Subtype - Immunology - Pathogenicityen_US
dc.subject.meshInfluenza A Virus, H5n1 Subtype - Immunology - Pathogenicityen_US
dc.subject.meshMacrophages - Metabolism - Virologyen_US
dc.subject.meshRna, Messenger - Genetics - Metabolismen_US
dc.subject.meshSwineen_US
dc.titleCytokine profiles induced by the novel swine-origin influenza A/H1N1 virus: Implications for treatment strategiesen_US
dc.typeArticleen_US
dc.identifier.emailWoo, PCY:pcywoo@hkucc.hku.hken_US
dc.identifier.emailLau, SKP:skplau@hkucc.hku.hken_US
dc.identifier.emailYuen, KY:kyyuen@hkucc.hku.hken_US
dc.identifier.authorityWoo, PCY=rp00430en_US
dc.identifier.authorityLau, SKP=rp00486en_US
dc.identifier.authorityYuen, KY=rp00366en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1086/649785en_US
dc.identifier.pmid20030555-
dc.identifier.scopuseid_2-s2.0-75649096767en_US
dc.identifier.hkuros171965-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-75649096767&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume201en_US
dc.identifier.issue3en_US
dc.identifier.spage346en_US
dc.identifier.epage353en_US
dc.identifier.isiWOS:000273441000006-
dc.publisher.placeUnited Statesen_US
dc.identifier.f10002860957-
dc.identifier.scopusauthoridWoo, PCY=7201801340en_US
dc.identifier.scopusauthoridTung, ETK=23398349800en_US
dc.identifier.scopusauthoridChan, KH=7406034307en_US
dc.identifier.scopusauthoridLau, CCY=8398162900en_US
dc.identifier.scopusauthoridLau, SKP=7401596211en_US
dc.identifier.scopusauthoridYuen, KY=36078079100en_US
dc.identifier.citeulike6433333-

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