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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, M3
Tipoe, GL1
Lau, YL1
Poon, LLM1
Ip, NY2
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
2012 Impact Factor: 5.848
2012 SCImago Journal Rankings: 2.723
 
DOIhttp://dx.doi.org/10.1086/590499
 
ISI Accession Number IDWOS:000257893300010
 
ReferencesReferences in Scopus
 
DC FieldValue
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
2012 Impact Factor: 5.848
2012 SCImago Journal Rankings: 2.723
 
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
 
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<contributor.author>Lau, YL</contributor.author>
<contributor.author>Poon, LLM</contributor.author>
<contributor.author>Ip, NY</contributor.author>
<contributor.author>Guan, Y</contributor.author>
<contributor.author>Peiris, JSM</contributor.author>
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<description.abstract>The 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 &#945; 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. &#169; 2008 by the Infectious Diseases Society of America. All rights reserved.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong
  2. Hong Kong University of Science and Technology
  3. Faculty of Medicine, Siriraj Hospital, Mahidol University