Tumor Necrosis Factor Alpha Enhances Influenza A Virus-Induced Expression of Antiviral Cytokines by Activating RIG-I Gene Expression

Sampsa Matikainen; Jukka Sirén; Jorma Tissari; Ville Veckman; Jaana Pirhonen; Martina Severa; Qiang Sun; Rongtuan Lin; Seppo Meri; Gilles Uzé; John Hiscott; Ilkka Julkunen

doi:10.1128/JVI.80.7.3515-3522.2006

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Tumor Necrosis Factor Alpha Enhances Influenza A Virus-Induced Expression of Antiviral Cytokines by Activating RIG-I Gene Expression

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Tumor Necrosis Factor Alpha Enhances Influenza A Virus-Induced Expression of Antiviral Cytokines by Activating RIG-I Gene Expression

Sampsa Matikainen, Jukka Sirén, Jorma Tissari, Ville Veckman, Jaana Pirhonen, Martina Severa, Qiang Sun, Rongtuan Lin, Seppo Meri, Gilles Uzé, …

Journal of virology, Vol.80(7), pp.3515-3522

01/04/2006

DOI: https://doi.org/10.1128/JVI.80.7.3515-3522.2006

PMID: 16537619

Résumé

Cellular Response to Infection

Epithelial cells of the lung are the primary targets for respiratory viruses. Virus-carried single-stranded RNA (ssRNA) can activate Toll-like receptors (TLRs) 7 and 8, whereas dsRNA is bound by TLR3 and a cytoplasmic RNA helicase, retinoic acid-inducible protein I (RIG-I). This recognition leads to the activation of host cell cytokine gene expression. Here we have studied the regulation of influenza A and Sendai virus-induced alpha interferon (IFN-α), IFN-β, interleukin-28 (IL-28), and IL-29 gene expression in human lung A549 epithelial cells. Sendai virus infection readily activated the expression of the IFN-α, IFN-β, IL-28, and IL-29 genes, whereas influenza A virus-induced activation of these genes was mainly dependent on pretreatment of A549 cells with IFN-α or tumor necrosis factor alpha (TNF-α). IFN-α and TNF-α induced the expression of the RIG-I, TLR3, MyD88, TRIF, and IRF7 genes, whereas no detectable TLR7 and TLR8 was seen in A549 cells. TNF-α also strongly enhanced IKKɛ mRNA and protein expression. Ectopic expression of a constitutively active form of RIG-I (ΔRIG-I) or IKKɛ, but not that of TLR3, enhanced the expression of the IFN-β, IL-28, and IL-29 genes. Furthermore, a dominant-negative form of RIG-I inhibited influenza A virus-induced IFN-β promoter activity in TNF-α-pretreated cells. In conclusion, IFN-α and TNF-α enhanced the expression of the components of TLR and RIG-I signaling pathways, but RIG-I was identified as the central regulator of influenza A virus-induced expression of antiviral cytokines in human lung epithelial cells.

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Titre: Tumor Necrosis Factor Alpha Enhances Influenza A Virus-Induced Expression of Antiviral Cytokines by Activating RIG-I Gene Expression
Créateurs - sans rôle: Sampsa Matikainen - Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland, Haartman Institute, Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland, Department of Infectious, Parasitic, and Immunomediated Diseases, Istituto Superiore di Sanità, Rome, Italy, Centre National de la Recherche Scientifique, Institute of Molecular Genetics, Montpellier, France, McGill University, Montreal, Canada
Jukka Sirén - Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland, Haartman Institute, Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland, Department of Infectious, Parasitic, and Immunomediated Diseases, Istituto Superiore di Sanità, Rome, Italy, Centre National de la Recherche Scientifique, Institute of Molecular Genetics, Montpellier, France, McGill University, Montreal, Canada
Jorma Tissari - Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland, Haartman Institute, Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland, Department of Infectious, Parasitic, and Immunomediated Diseases, Istituto Superiore di Sanità, Rome, Italy, Centre National de la Recherche Scientifique, Institute of Molecular Genetics, Montpellier, France, McGill University, Montreal, Canada
Ville Veckman - Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland, Haartman Institute, Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland, Department of Infectious, Parasitic, and Immunomediated Diseases, Istituto Superiore di Sanità, Rome, Italy, Centre National de la Recherche Scientifique, Institute of Molecular Genetics, Montpellier, France, McGill University, Montreal, Canada
Jaana Pirhonen - Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland, Haartman Institute, Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland, Department of Infectious, Parasitic, and Immunomediated Diseases, Istituto Superiore di Sanità, Rome, Italy, Centre National de la Recherche Scientifique, Institute of Molecular Genetics, Montpellier, France, McGill University, Montreal, Canada
Martina Severa - Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland, Haartman Institute, Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland, Department of Infectious, Parasitic, and Immunomediated Diseases, Istituto Superiore di Sanità, Rome, Italy, Centre National de la Recherche Scientifique, Institute of Molecular Genetics, Montpellier, France, McGill University, Montreal, Canada
Qiang Sun - Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland, Haartman Institute, Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland, Department of Infectious, Parasitic, and Immunomediated Diseases, Istituto Superiore di Sanità, Rome, Italy, Centre National de la Recherche Scientifique, Institute of Molecular Genetics, Montpellier, France, McGill University, Montreal, Canada
Rongtuan Lin - McGill University
Seppo Meri - Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland, Haartman Institute, Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland, Department of Infectious, Parasitic, and Immunomediated Diseases, Istituto Superiore di Sanità, Rome, Italy, Centre National de la Recherche Scientifique, Institute of Molecular Genetics, Montpellier, France, McGill University, Montreal, Canada
Gilles Uzé - Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland, Haartman Institute, Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland, Department of Infectious, Parasitic, and Immunomediated Diseases, Istituto Superiore di Sanità, Rome, Italy, Centre National de la Recherche Scientifique, Institute of Molecular Genetics, Montpellier, France, McGill University, Montreal, Canada
John Hiscott - Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland, Haartman Institute, Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland, Department of Infectious, Parasitic, and Immunomediated Diseases, Istituto Superiore di Sanità, Rome, Italy, Centre National de la Recherche Scientifique, Institute of Molecular Genetics, Montpellier, France, McGill University, Montreal, Canada
Ilkka Julkunen - Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland, Haartman Institute, Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland, Department of Infectious, Parasitic, and Immunomediated Diseases, Istituto Superiore di Sanità, Rome, Italy, Centre National de la Recherche Scientifique, Institute of Molecular Genetics, Montpellier, France, McGill University, Montreal, Canada
Détails de publication: Journal of virology, Vol.80(7), pp.3515-3522
Éditeur: American Society for Microbiology
Nombre de pages: 8
Identifiants: 99155729809311
Unité académique: Cell souches plasticité cellul régénérat tissulaire immuno des maladies inflamm - IRMB
Langue: English
Type de ressource: Journal article