Article: Hyperinduction of cyclooxygenase-2-mediated proinflammatory cascade: A mechanism for the pathogenesis of avian influenza H5N1 infection

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TitleHyperinduction of cyclooxygenase-2-mediated proinflammatory cascade: A mechanism for the pathogenesis of avian influenza H5N1 infection
AuthorsLee, SMY1
Cheung, CY1
Nicholls, JM1
Hui, KPY1
Leung, CYH1
Uiprasertkul, M2
Tipoe, GL1
Lau, YL1
Poon, LLM1
Ip, NY3
Guan, Y1
Peiris, JSM1
KeywordsChemicals And Cas Registry Numbers
Issue Date2008
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
CitationJournal Of Infectious Diseases, 2008, v. 198 n. 4, p. 525-535 [How to Cite?]
DOI: http://dx.doi.org/10.1086/590499
AbstractThe mechanism for the pathogenesis of H5N1 infection in humans remains unclear. This study reveals that cyclooxygenase-2 (COX-2) was strongly induced in H5N1-infected macrophages in vitro and in epithelial cells of lung tissue samples obtained during autopsy of patients who died of H5N1 disease. Novel findings demonstrated that COX-2, along with tumor necrosis factor α and other proinflammatory cytokines were hyperinduced in epithelial cells by secretory factors from H5N1-infected macrophages in vitro. This amplification of the proinflammatory response is rapid, and the effects elicited by the H5N1-triggered proinflammatory cascade are broader than those arising from direct viral infection. Furthermore, selective COX-2 inhibitors suppress the hyperinduction of cytokines in the proinflammatory cascade, indicating a regulatory role for COX-2 in the H5N1-hyperinduced host proinflammatory cascade. These data provide a basis for the possible development of novel therapeutic interventions for the treatment of H5N1 disease, as adjuncts to antiviral drugs. © 2008 by the Infectious Diseases Society of America. All rights reserved.
ISSN0022-1899
2011 Impact Factor: 6.41
2011 SCImago Journal Rankings: 0.831
DOIhttp://dx.doi.org/10.1086/590499
ISI Accession Number IDWOS:000257893300010
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorLee, SMY
dc.contributor.authorCheung, CY
dc.contributor.authorNicholls, JM
dc.contributor.authorHui, KPY
dc.contributor.authorLeung, CYH
dc.contributor.authorUiprasertkul, M
dc.contributor.authorTipoe, GL
dc.contributor.authorLau, YL
dc.contributor.authorPoon, LLM
dc.contributor.authorIp, NY
dc.contributor.authorGuan, Y
dc.contributor.authorPeiris, JSM
dc.date.accessioned2011-09-27T02:59:25Z
dc.date.available2011-09-27T02:59:25Z
dc.date.issued2008
dc.description.abstractThe mechanism for the pathogenesis of H5N1 infection in humans remains unclear. This study reveals that cyclooxygenase-2 (COX-2) was strongly induced in H5N1-infected macrophages in vitro and in epithelial cells of lung tissue samples obtained during autopsy of patients who died of H5N1 disease. Novel findings demonstrated that COX-2, along with tumor necrosis factor α and other proinflammatory cytokines were hyperinduced in epithelial cells by secretory factors from H5N1-infected macrophages in vitro. This amplification of the proinflammatory response is rapid, and the effects elicited by the H5N1-triggered proinflammatory cascade are broader than those arising from direct viral infection. Furthermore, selective COX-2 inhibitors suppress the hyperinduction of cytokines in the proinflammatory cascade, indicating a regulatory role for COX-2 in the H5N1-hyperinduced host proinflammatory cascade. These data provide a basis for the possible development of novel therapeutic interventions for the treatment of H5N1 disease, as adjuncts to antiviral drugs. © 2008 by the Infectious Diseases Society of America. All rights reserved.
dc.description.naturelink_to_subscribed_fulltext
dc.identifier.citationJournal Of Infectious Diseases, 2008, v. 198 n. 4, p. 525-535 [How to Cite?]
DOI: http://dx.doi.org/10.1086/590499
dc.identifier.doihttp://dx.doi.org/10.1086/590499
dc.identifier.epage535
dc.identifier.hkuros146550
dc.identifier.isiWOS:000257893300010
dc.identifier.issn0022-1899
2011 Impact Factor: 6.41
2011 SCImago Journal Rankings: 0.831
dc.identifier.issue4
dc.identifier.pmid18613795
dc.identifier.scopuseid_2-s2.0-48749089085
dc.identifier.spage525
dc.identifier.urihttp://hdl.handle.net/10722/141724
dc.identifier.volume198
dc.languageeng
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
dc.publisher.placeUnited States
dc.relation.ispartofJournal of Infectious Diseases
dc.relation.referencesReferences in Scopus
dc.subject.meshAnimals
dc.subject.meshBirds
dc.subject.meshCyclooxygenase 2 - biosynthesis - genetics
dc.subject.meshCyclooxygenase 2 Inhibitors
dc.subject.meshHumans
dc.subject.meshInfluenza A Virus, H5N1 Subtype - genetics - immunology - pathogenicity
dc.subject.meshInfluenza in Birds - enzymology - immunology - virology
dc.subject.meshInfluenza, Human - enzymology - virology
dc.subjectChemicals And Cas Registry Numbers
dc.titleHyperinduction of cyclooxygenase-2-mediated proinflammatory cascade: A mechanism for the pathogenesis of avian influenza H5N1 infection
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong
  2. Faculty of Medicine, Siriraj Hospital, Mahidol University
  3. Hong Kong University of Science and Technology