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Article: H5N1 influenza virus-induced mediators upregulate RIG-I in uninfected cells by paracrine effects contributing to amplified cytokine cascades
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TitleH5N1 influenza virus-induced mediators upregulate RIG-I in uninfected cells by paracrine effects contributing to amplified cytokine cascades
 
AuthorsHui, KPY1
Lee, SMY1
Cheung, CY1
Mao, H1
Lai, AKW1
Chan, RWY1
Chan, MCW1
Tu, W1
Guan, Y1
Lau, YL1
Peiris, JSM1 2
 
Issue Date2011
 
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
 
CitationJournal Of Infectious Diseases, 2011, v. 204 n. 12, p. 1866-1878 [How to Cite?]
DOI: http://dx.doi.org/10.1093/infdis/jir665
 
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.
 
ISSN0022-1899
2013 Impact Factor: 5.778
 
DOIhttp://dx.doi.org/10.1093/infdis/jir665
 
ISI Accession Number IDWOS:000297069100009
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).

 
ReferencesReferences in Scopus
 
GrantsRole 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 FieldValue
dc.contributor.authorHui, KPY
 
dc.contributor.authorLee, SMY
 
dc.contributor.authorCheung, CY
 
dc.contributor.authorMao, H
 
dc.contributor.authorLai, AKW
 
dc.contributor.authorChan, RWY
 
dc.contributor.authorChan, MCW
 
dc.contributor.authorTu, W
 
dc.contributor.authorGuan, Y
 
dc.contributor.authorLau, YL
 
dc.contributor.authorPeiris, JSM
 
dc.date.accessioned2012-04-20T02:05:13Z
 
dc.date.available2012-04-20T02:05:13Z
 
dc.date.issued2011
 
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.
 
dc.description.natureLink_to_OA_fulltext
 
dc.identifier.citationJournal Of Infectious Diseases, 2011, v. 204 n. 12, p. 1866-1878 [How to Cite?]
DOI: http://dx.doi.org/10.1093/infdis/jir665
 
dc.identifier.doihttp://dx.doi.org/10.1093/infdis/jir665
 
dc.identifier.epage1878
 
dc.identifier.hkuros200729
 
dc.identifier.hkuros202477
 
dc.identifier.isiWOS:000297069100009
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).

 
dc.identifier.issn0022-1899
2013 Impact Factor: 5.778
 
dc.identifier.issue12
 
dc.identifier.pmid22013225
 
dc.identifier.scopuseid_2-s2.0-81055143878
 
dc.identifier.spage1866
 
dc.identifier.urihttp://hdl.handle.net/10722/146347
 
dc.identifier.volume204
 
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.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.relation.referencesReferences in Scopus
 
dc.subject.meshAdaptor Proteins, Signal Transducing - genetics - immunology - metabolism
 
dc.subject.meshCells, Cultured
 
dc.subject.meshCytokines - metabolism
 
dc.subject.meshDEAD-box RNA Helicases - genetics - immunology - metabolism
 
dc.subject.meshEpithelial Cells - immunology - metabolism
 
dc.subject.meshHumans
 
dc.subject.meshImmunity, Innate
 
dc.subject.meshInfluenza A Virus, H1N1 Subtype - genetics - immunology
 
dc.subject.meshInfluenza A Virus, H5N1 Subtype - genetics - immunology
 
dc.subject.meshInfluenza, Human - immunology - metabolism - virology
 
dc.subject.meshInterferon Regulatory Factor-3 - metabolism
 
dc.subject.meshJanus Kinases - immunology
 
dc.subject.meshMacrophages - immunology - metabolism
 
dc.subject.meshNF-kappa B - metabolism
 
dc.subject.meshParacrine Communication - immunology
 
dc.subject.meshPulmonary Alveoli - immunology - metabolism
 
dc.subject.meshRNA, Small Interfering - genetics
 
dc.subject.meshRNA, Viral - metabolism
 
dc.subject.meshReceptor, Interferon alpha-beta - immunology
 
dc.subject.meshSignal Transduction
 
dc.subject.meshToll-Like Receptor 3 - metabolism
 
dc.subject.meshUp-Regulation
 
dc.subject.meshp38 Mitogen-Activated Protein Kinases - metabolism
 
dc.titleH5N1 influenza virus-induced mediators upregulate RIG-I in uninfected cells by paracrine effects contributing to amplified cytokine cascades
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. HKU-Pasteur Research Centre