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Article: H5N1 influenza virus-induced mediators upregulate RIG-I in uninfected cells by paracrine effects contributing to amplified cytokine cascades

TitleH5N1 influenza virus-induced mediators upregulate RIG-I in uninfected cells by paracrine effects contributing to amplified cytokine cascades
Authors
Issue Date2011
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
Citation
Journal Of Infectious Diseases, 2011, v. 204 n. 12, p. 1866-1878 How to Cite?
Abstract
Highly pathogenic avian influenza H5N1 viruses cause severe disease in humans, and dysregulation of cytokine responses is believed to contribute to the pathogenesis of human H5N1 disease. However, mechanisms leading to the increased induction of proinflammatory cytokines by H5N1 viruses are poorly understood. We show that the innate sensing receptor RIG-I is involved in interferon regulatory factor 3 (IRF3), NF-κB nuclear translocation, p38 activation, and the subsequent interferon (IFN) β, IFN-λ1, and tumor necrosis factor α induction during H5N1 infection. Soluble mediators from H5N1-infected human macrophages upregulate RIG-I, MDA5, and TLR3 to much higher levels than those from seasonal H1N1 in uninfected human macrophages and alveolar epithelial cells via paracrine IFNAR1/JAK but not IFN-λ receptor signaling. Compared with H1N1 virus-induced mediators, H5N1 mediators markedly enhance the cytokine response to PolyIC and to both seasonal and H5N1 virus infection in a RIG-I-dependent manner. Thus, sensitizing neighboring cells by upregulation of RIG-I contributes to the amplified cytokine cascades during H5N1 infection. © 2011 The Author.
Persistent Identifierhttp://hdl.handle.net/10722/146347
ISSN
2013 Impact Factor: 5.778
ISI Accession Number ID
Funding AgencyGrant Number
Food and Health Bureau of Hong Kong SAR10091062
Research Grant Council of Hong Kong SAR7620/06M
Funding Information:

This work was supported by an RFCID grant (10091062) from the Food and Health Bureau of Hong Kong SAR and a grant from the Research Grant Council of Hong Kong SAR (7620/06M).

References
Grants

 

Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. HKU-Pasteur Research Centre
DC FieldValueLanguage
dc.contributor.authorHui, KPYen_HK
dc.contributor.authorLee, SMYen_HK
dc.contributor.authorCheung, CYen_HK
dc.contributor.authorMao, Hen_HK
dc.contributor.authorLai, AKWen_HK
dc.contributor.authorChan, RWYen_HK
dc.contributor.authorChan, MCWen_HK
dc.contributor.authorTu, Wen_HK
dc.contributor.authorGuan, Yen_HK
dc.contributor.authorLau, YLen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.date.accessioned2012-04-20T02:05:13Z-
dc.date.available2012-04-20T02:05:13Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Infectious Diseases, 2011, v. 204 n. 12, p. 1866-1878en_HK
dc.identifier.issn0022-1899en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146347-
dc.description.abstractHighly pathogenic avian influenza H5N1 viruses cause severe disease in humans, and dysregulation of cytokine responses is believed to contribute to the pathogenesis of human H5N1 disease. However, mechanisms leading to the increased induction of proinflammatory cytokines by H5N1 viruses are poorly understood. We show that the innate sensing receptor RIG-I is involved in interferon regulatory factor 3 (IRF3), NF-κB nuclear translocation, p38 activation, and the subsequent interferon (IFN) β, IFN-λ1, and tumor necrosis factor α induction during H5N1 infection. Soluble mediators from H5N1-infected human macrophages upregulate RIG-I, MDA5, and TLR3 to much higher levels than those from seasonal H1N1 in uninfected human macrophages and alveolar epithelial cells via paracrine IFNAR1/JAK but not IFN-λ receptor signaling. Compared with H1N1 virus-induced mediators, H5N1 mediators markedly enhance the cytokine response to PolyIC and to both seasonal and H5N1 virus infection in a RIG-I-dependent manner. Thus, sensitizing neighboring cells by upregulation of RIG-I contributes to the amplified cytokine cascades during H5N1 infection. © 2011 The Author.en_HK
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.orgen_HK
dc.relation.ispartofJournal of Infectious Diseasesen_HK
dc.subject.meshAdaptor Proteins, Signal Transducing - genetics - immunology - metabolismen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshCytokines - metabolismen_HK
dc.subject.meshDEAD-box RNA Helicases - genetics - immunology - metabolismen_HK
dc.subject.meshEpithelial Cells - immunology - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunity, Innateen_HK
dc.subject.meshInfluenza A Virus, H1N1 Subtype - genetics - immunologyen_HK
dc.subject.meshInfluenza A Virus, H5N1 Subtype - genetics - immunologyen_HK
dc.subject.meshInfluenza, Human - immunology - metabolism - virologyen_HK
dc.subject.meshInterferon Regulatory Factor-3 - metabolismen_HK
dc.subject.meshJanus Kinases - immunologyen_HK
dc.subject.meshMacrophages - immunology - metabolismen_HK
dc.subject.meshNF-kappa B - metabolismen_HK
dc.subject.meshParacrine Communication - immunologyen_HK
dc.subject.meshPulmonary Alveoli - immunology - metabolismen_HK
dc.subject.meshRNA, Small Interfering - geneticsen_HK
dc.subject.meshRNA, Viral - metabolismen_HK
dc.subject.meshReceptor, Interferon alpha-beta - immunologyen_HK
dc.subject.meshSignal Transductionen_HK
dc.subject.meshToll-Like Receptor 3 - metabolismen_HK
dc.subject.meshUp-Regulationen_HK
dc.subject.meshp38 Mitogen-Activated Protein Kinases - metabolismen_HK
dc.titleH5N1 influenza virus-induced mediators upregulate RIG-I in uninfected cells by paracrine effects contributing to amplified cytokine cascadesen_HK
dc.typeArticleen_HK
dc.identifier.emailLee, SMY: suki@hku.hken_HK
dc.identifier.emailCheung, CY: chungey@hkucc.hku.hken_HK
dc.identifier.emailMao, H: hwmau@hku.hken_HK
dc.identifier.emailChan, RWY: reneewy@hku.hken_HK
dc.identifier.emailChan, MCW: mchan@hku.hken_HK
dc.identifier.emailTu, W: wwtu@hku.hken_HK
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hken_HK
dc.identifier.emailLau, YL: lauylung@hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.authorityLee, SMY=rp01536en_HK
dc.identifier.authorityCheung, CY=rp00404en_HK
dc.identifier.authorityMao, H=rp01595en_HK
dc.identifier.authorityChan, RWY=rp01596en_HK
dc.identifier.authorityChan, MCW=rp00420en_HK
dc.identifier.authorityTu, W=rp00416en_HK
dc.identifier.authorityGuan, Y=rp00397en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1093/infdis/jir665en_HK
dc.identifier.pmid22013225en_HK
dc.identifier.scopuseid_2-s2.0-81055143878en_HK
dc.identifier.hkuros200729-
dc.identifier.hkuros202477-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-81055143878&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume204en_HK
dc.identifier.issue12en_HK
dc.identifier.spage1866en_HK
dc.identifier.epage1878en_HK
dc.identifier.isiWOS:000297069100009-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectRole of retinoic acid inducible gene-1, toll-like receptor-3 and -8 in cytokine induction by influenza A H5N1 and pandemic H1N1 viruses in primary human cells-
dc.identifier.scopusauthoridHui, KPY=24492032000en_HK
dc.identifier.scopusauthoridLee, SMY=35435155600en_HK
dc.identifier.scopusauthoridCheung, CY=7202061836en_HK
dc.identifier.scopusauthoridMao, H=25632489000en_HK
dc.identifier.scopusauthoridLai, AKW=54780072700en_HK
dc.identifier.scopusauthoridChan, RWY=26661379100en_HK
dc.identifier.scopusauthoridChan, MCW=26654715500en_HK
dc.identifier.scopusauthoridTu, W=7006479236en_HK
dc.identifier.scopusauthoridGuan, Y=7202924055en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK

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