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Conference Paper: The role of interferon regulatory factor 3 and p38 in influenza a virus induced pro-inflammatory cytokines

TitleThe role of interferon regulatory factor 3 and p38 in influenza a virus induced pro-inflammatory cytokines
Authors
Issue Date2008
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/cytokine
Citation
The 7th Joint Conference of the International Cytokine Society and the International Society for Interferon and Cytokine Research, Montreal, Quebec, 12-16 October 2008. In Cytokine, 2008, v. 43 n. 3, p. 259 How to Cite?
AbstractThe hyperinduction of pro-inflammatory cytokines and chemokines such as TNF-α, IFN-β, and CCL2/MCP-1 in primary human macrophages by the highly pathogenic avian influenza H5N1 is believed to contribute to the unusual severity of human H5N1 disease. Here we show that TNF-α and IFN-β are the key mediators directly induced by the H5N1 virus in primary human macrophages. In comparison to human influenza (H1N1), the H5N1 virus more strongly activated interferon regulatory factor 3 (IRF3). IRF3 knock-down and p38 kinase inhibition separately and in combination led to a dramatic reduction of IFN-β and MCP-1 but only to a partial reduction of TNF-α. IRF3 translocation was independent of p38 activity indicating that IRF3 and p38 are distinct pathways leading to cytokine production by H5N1 virus. We conclude that IRF3 and p38 kinase separately and predominantly contribute to H5N1-mediated hyper-induction of IFN-β and MCP-1 but only partly control TNF-α induction. A more precise identification of the differences in the regulation of TNF-α and IFN-β may provide novel strategies for the design of therapeutic strategies for severe human H5N1 influenza and also for treating other causes of acute respiratory disease syndrome.
Persistent Identifierhttp://hdl.handle.net/10722/62477
ISSN
2015 Impact Factor: 2.94
2015 SCImago Journal Rankings: 1.294
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHui, PYen_HK
dc.contributor.authorLee, MYen_HK
dc.contributor.authorCheung, CYen_HK
dc.contributor.authorNg, IHYen_HK
dc.contributor.authorPoon, LLM-
dc.contributor.authorGuan, Y-
dc.contributor.authorIp, NY-
dc.contributor.authorLau, ASY-
dc.contributor.authorPeiris, JSM-
dc.date.accessioned2010-07-13T04:02:09Z-
dc.date.available2010-07-13T04:02:09Z-
dc.date.issued2008en_HK
dc.identifier.citationThe 7th Joint Conference of the International Cytokine Society and the International Society for Interferon and Cytokine Research, Montreal, Quebec, 12-16 October 2008. In Cytokine, 2008, v. 43 n. 3, p. 259en_HK
dc.identifier.issn1043-4666en_HK
dc.identifier.urihttp://hdl.handle.net/10722/62477-
dc.description.abstractThe hyperinduction of pro-inflammatory cytokines and chemokines such as TNF-α, IFN-β, and CCL2/MCP-1 in primary human macrophages by the highly pathogenic avian influenza H5N1 is believed to contribute to the unusual severity of human H5N1 disease. Here we show that TNF-α and IFN-β are the key mediators directly induced by the H5N1 virus in primary human macrophages. In comparison to human influenza (H1N1), the H5N1 virus more strongly activated interferon regulatory factor 3 (IRF3). IRF3 knock-down and p38 kinase inhibition separately and in combination led to a dramatic reduction of IFN-β and MCP-1 but only to a partial reduction of TNF-α. IRF3 translocation was independent of p38 activity indicating that IRF3 and p38 are distinct pathways leading to cytokine production by H5N1 virus. We conclude that IRF3 and p38 kinase separately and predominantly contribute to H5N1-mediated hyper-induction of IFN-β and MCP-1 but only partly control TNF-α induction. A more precise identification of the differences in the regulation of TNF-α and IFN-β may provide novel strategies for the design of therapeutic strategies for severe human H5N1 influenza and also for treating other causes of acute respiratory disease syndrome.-
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/cytokineen_HK
dc.relation.ispartofCytokine-
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in Cytokine. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Cytokine, [VOL 43, ISSUE 3, 2008] DOI 10.1016/j.cyto.2008.07.142-
dc.titleThe role of interferon regulatory factor 3 and p38 in influenza a virus induced pro-inflammatory cytokinesen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailHui, PY: yanhui@graduate.hku.hken_HK
dc.identifier.emailLee, MY: myleesuki01@yahoo.com.hken_HK
dc.identifier.emailCheung, CY: chungey@hkucc.hku.hken_HK
dc.identifier.emailNg, IHY: irishyng@yahoo.comen_HK
dc.identifier.emailPoon, LLM: llmpoon@hkucc.hku.hk-
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hk-
dc.identifier.emailLau, ASY: asylau@hku.hk-
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hk-
dc.identifier.authorityLee, MY=rp01536en_HK
dc.identifier.authorityCheung, CY=rp00404en_HK
dc.description.natureabstract-
dc.identifier.doi10.1016/j.cyto.2008.07.142-
dc.identifier.hkuros165211en_HK
dc.identifier.volume43-
dc.identifier.issue3-
dc.identifier.spage259-
dc.identifier.epage259-
dc.identifier.isiWOS:000260212900120-
dc.publisher.placeUnited Kingdom-
dc.description.otherThe 7th Joint Conference of the International Cytokine Society and the International Society for Interferon and Cytokine Research, Montreal, Quebec, 12–16 October 2008. In Cytokine, 2008, v. 43 n. 3, p. 259-

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