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Conference Paper: Induction of pro-inflammatory mediators by H5N1 infection of primary human lung microvascular endothelial cells

TitleInduction of pro-inflammatory mediators by H5N1 infection of primary human lung microvascular endothelial cells
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 influenza virus H5N1 cause the devastating “bird flu” outbreaks in domestic fowl, but are also occasionally the cause of human disease with a high mortality rate. Infection in birds is systemic with hemorrhages and edema as characteristic symptoms, and virus replication in the endothelium appears to play an important role in pathogenesis, whereas this role for pathogenesis in humans remained uncertain. There is much evidence to suggest that an excessive proinflammatory reaction elicited by H5N1 viruses may be important contributor to H5N1 pathogenesis. In this study we demonstrated that H5N1 enters and replicates in human endothelial cells, but the level of replication is either abortive or too low for infectious particles to be detected. A range of proinflammatory mediators were induced including COX-2, TNF-alpha, IL-1 beta, CXCL10/IP-10, and CCL5/RANTES. Indeed the range of cytokine induction is wider than that of H5N1 infected epithelial cells. Hence lung endothelial cells may not significantly contribute to H5N1 replication as in avian species, however endothelial cells does appears to be important contributor to the proinflammatory cascade that ensues upon H5N1 infection in the respiratory system.
Persistent Identifierhttp://hdl.handle.net/10722/62467
ISSN
2015 Impact Factor: 2.94
2015 SCImago Journal Rankings: 1.294
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCheung, CYen_HK
dc.contributor.authorLee, MYen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.date.accessioned2010-07-13T04:01:56Z-
dc.date.available2010-07-13T04:01:56Z-
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/10722/62467-
dc.description.abstractHighly pathogenic avian influenza virus H5N1 cause the devastating “bird flu” outbreaks in domestic fowl, but are also occasionally the cause of human disease with a high mortality rate. Infection in birds is systemic with hemorrhages and edema as characteristic symptoms, and virus replication in the endothelium appears to play an important role in pathogenesis, whereas this role for pathogenesis in humans remained uncertain. There is much evidence to suggest that an excessive proinflammatory reaction elicited by H5N1 viruses may be important contributor to H5N1 pathogenesis. In this study we demonstrated that H5N1 enters and replicates in human endothelial cells, but the level of replication is either abortive or too low for infectious particles to be detected. A range of proinflammatory mediators were induced including COX-2, TNF-alpha, IL-1 beta, CXCL10/IP-10, and CCL5/RANTES. Indeed the range of cytokine induction is wider than that of H5N1 infected epithelial cells. Hence lung endothelial cells may not significantly contribute to H5N1 replication as in avian species, however endothelial cells does appears to be important contributor to the proinflammatory cascade that ensues upon H5N1 infection in the respiratory system.-
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.2008.07.140-
dc.titleInduction of pro-inflammatory mediators by H5N1 infection of primary human lung microvascular endothelial cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailCheung, CY: chungey@hkucc.hku.hken_HK
dc.identifier.emailLee, MY: myleesuki01@yahoo.com.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.authorityCheung, CY=rp00404en_HK
dc.identifier.authorityLee, MY=rp01536en_HK
dc.description.natureabstract-
dc.identifier.doi10.1016/j.cyto.2008.07.140-
dc.identifier.hkuros165207en_HK
dc.identifier.volume43-
dc.identifier.issue3-
dc.identifier.spage259-
dc.identifier.epage259-
dc.identifier.isiWOS:000260212900118-
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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