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Conference Paper: Hyper-induction of COX-2-medicated proinflammatory cascade: A mechanism for the pathogenesis of avian influenza H5N1 infection

TitleHyper-induction of COX-2-medicated proinflammatory cascade: A mechanism for the pathogenesis of avian influenza H5N1 infection
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?
AbstractHighly pathogenic avian virus H5N1 continues to pose a serious threat to human health. It is therefore important to understand its pathogenesis and to explore novel therapeutic options. Recent studies have demonstrated that the intense proinflammatory response may be a major contributory factor to the pathogenesis of this virus. In this study, we found that COX-2 was strongly induced in H5N1-infected macrophages and in epithelial cells in autopsy lung-tissue from patients dying of H5N1 disease. COX-2, along with TNF-α and other proinflammatory cytokines, were found to be hyper-induced in epithelial cells by secretory factors from H5N1-infected human macrophages in vitro and contribute to the amplification of the proinflammatory response. This amplification is rapid, and the effects elicited by H5N1-triggered proinflammatory cascade are broader than those arising from direct viral infection. Furthermore, selective COX-2 inhibitors were able to suppress the hyper-induction of cytokines in the proinflammatory cascade, indicating a regulatory role for COX-2 in the H5N1 hyper-induced host proinflammatory cascade. Taken together, these results highlight the role of the host proinflammatory response in the pathogenesis of H5N1 infection and may indicate a novel therapeutic option for the treatment of H5N1 disease, as an adjunct to antiviral drugs.
Persistent Identifierhttp://hdl.handle.net/10722/62468
ISSN
2015 Impact Factor: 2.94
2015 SCImago Journal Rankings: 1.294
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLee, MYen_HK
dc.contributor.authorCheung, CYen_HK
dc.contributor.authorNicholls, JMen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.date.accessioned2010-07-13T04:01:57Z-
dc.date.available2010-07-13T04:01:57Z-
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/10722/62468-
dc.description.abstractHighly pathogenic avian virus H5N1 continues to pose a serious threat to human health. It is therefore important to understand its pathogenesis and to explore novel therapeutic options. Recent studies have demonstrated that the intense proinflammatory response may be a major contributory factor to the pathogenesis of this virus. In this study, we found that COX-2 was strongly induced in H5N1-infected macrophages and in epithelial cells in autopsy lung-tissue from patients dying of H5N1 disease. COX-2, along with TNF-α and other proinflammatory cytokines, were found to be hyper-induced in epithelial cells by secretory factors from H5N1-infected human macrophages in vitro and contribute to the amplification of the proinflammatory response. This amplification is rapid, and the effects elicited by H5N1-triggered proinflammatory cascade are broader than those arising from direct viral infection. Furthermore, selective COX-2 inhibitors were able to suppress the hyper-induction of cytokines in the proinflammatory cascade, indicating a regulatory role for COX-2 in the H5N1 hyper-induced host proinflammatory cascade. Taken together, these results highlight the role of the host proinflammatory response in the pathogenesis of H5N1 infection and may indicate a novel therapeutic option for the treatment of H5N1 disease, as an adjunct to antiviral drugs.-
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.2008.07.139-
dc.titleHyper-induction of COX-2-medicated proinflammatory cascade: A mechanism for the pathogenesis of avian influenza H5N1 infectionen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLee, MY: myleesuki01@yahoo.com.hken_HK
dc.identifier.emailCheung, CY: chungey@hkucc.hku.hken_HK
dc.identifier.emailNicholls, JM: nicholls@pathology.hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.authorityLee, MY=rp01536en_HK
dc.identifier.authorityCheung, CY=rp00404en_HK
dc.identifier.authorityNicholls, JM=rp00364en_HK
dc.description.natureabstract-
dc.identifier.doi10.1016/j.cyto.2008.07.139-
dc.identifier.hkuros165214en_HK
dc.identifier.volume43-
dc.identifier.issue3-
dc.identifier.spage259-
dc.identifier.epage259-
dc.identifier.isiWOS:000260212900117-
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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