Requirement of NOX2 and Reactive Oxygen Species for Efficient RIG-I-Mediated Antiviral Response through Regulation of MAVS Expression
The innate immune response is essential to the host defense against viruses, through restriction of virus replication and coordination of the adaptive immune response. Induction of antiviral genes is a tightly regulated process initiated mainly through sensing of invading virus nucleic acids in the...
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| Published in | PLoS pathogens Vol. 6; no. 6; p. e1000930 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
01.06.2010
Public Library of Science (PLoS) |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1553-7374 1553-7366 1553-7374 |
| DOI | 10.1371/journal.ppat.1000930 |
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| Abstract | The innate immune response is essential to the host defense against viruses, through restriction of virus replication and coordination of the adaptive immune response. Induction of antiviral genes is a tightly regulated process initiated mainly through sensing of invading virus nucleic acids in the cytoplasm by RIG-I like helicases, RIG-I or Mda5, which transmit the signal through a common mitochondria-associated adaptor, MAVS. Although major breakthroughs have recently been made, much remains unknown about the mechanisms that translate virus recognition into antiviral genes expression. Beside the reputed detrimental role, reactive oxygen species (ROS) act as modulators of cellular signaling and gene regulation. NADPH oxidase (NOX) enzymes are a main source of deliberate cellular ROS production. Here, we found that NOX2 and ROS are required for the host cell to trigger an efficient RIG-I-mediated IRF-3 activation and downstream antiviral IFNbeta and IFIT1 gene expression. Additionally, we provide evidence that NOX2 is critical for the expression of the central mitochondria-associated adaptor MAVS. Taken together these data reveal a new facet to the regulation of the innate host defense against viruses through the identification of an unrecognized role of NOX2 and ROS. |
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| AbstractList | The innate immune response is essential to the host defense against viruses, through restriction of virus replication and coordination of the adaptive immune response. Induction of antiviral genes is a tightly regulated process initiated mainly through sensing of invading virus nucleic acids in the cytoplasm by RIG-I like helicases, RIG-I or Mda5, which transmit the signal through a common mitochondria-associated adaptor, MAVS. Although major breakthroughs have recently been made, much remains unknown about the mechanisms that translate virus recognition into antiviral genes expression. Beside the reputed detrimental role, reactive oxygen species (ROS) act as modulators of cellular signaling and gene regulation. NADPH oxidase (NOX) enzymes are a main source of deliberate cellular ROS production. Here, we found that NOX2 and ROS are required for the host cell to trigger an efficient RIG-I-mediated IRF-3 activation and downstream antiviral IFNbeta and IFIT1 gene expression. Additionally, we provide evidence that NOX2 is critical for the expression of the central mitochondria-associated adaptor MAVS. Taken together these data reveal a new facet to the regulation of the innate host defense against viruses through the identification of an unrecognized role of NOX2 and ROS.The innate immune response is essential to the host defense against viruses, through restriction of virus replication and coordination of the adaptive immune response. Induction of antiviral genes is a tightly regulated process initiated mainly through sensing of invading virus nucleic acids in the cytoplasm by RIG-I like helicases, RIG-I or Mda5, which transmit the signal through a common mitochondria-associated adaptor, MAVS. Although major breakthroughs have recently been made, much remains unknown about the mechanisms that translate virus recognition into antiviral genes expression. Beside the reputed detrimental role, reactive oxygen species (ROS) act as modulators of cellular signaling and gene regulation. NADPH oxidase (NOX) enzymes are a main source of deliberate cellular ROS production. Here, we found that NOX2 and ROS are required for the host cell to trigger an efficient RIG-I-mediated IRF-3 activation and downstream antiviral IFNbeta and IFIT1 gene expression. Additionally, we provide evidence that NOX2 is critical for the expression of the central mitochondria-associated adaptor MAVS. Taken together these data reveal a new facet to the regulation of the innate host defense against viruses through the identification of an unrecognized role of NOX2 and ROS. The innate immune response is essential to the host defense against viruses, through restriction of virus replication and coordination of the adaptive immune response. Induction of antiviral genes is a tightly regulated process initiated mainly through sensing of invading virus nucleic acids in the cytoplasm by RIG-I like helicases, RIG-I or Mda5, which transmit the signal through a common mitochondria-associated adaptor, MAVS. Although major breakthroughs have recently been made, much remains unknown about the mechanisms that translate virus recognition into antiviral genes expression. Beside the reputed detrimental role, reactive oxygen species (ROS) act as modulators of cellular signaling and gene regulation. NADPH oxidase (NOX) enzymes are a main source of deliberate cellular ROS production. Here, we found that NOX2 and ROS are required for the host cell to trigger an efficient RIG-I-mediated IRF-3 activation and downstream antiviral IFNβ and IFIT1 gene expression. Additionally, we provide evidence that NOX2 is critical for the expression of the central mitochondria-associated adaptor MAVS. Taken together these data reveal a new facet to the regulation of the innate host defense against viruses through the identification of an unrecognized role of NOX2 and ROS. The innate immune response is essential to the host defense against viruses, through restriction of virus replication and coordination of the adaptive immune response. Induction of antiviral genes is a tightly regulated process initiated mainly through sensing of invading virus nucleic acids in the cytoplasm by RIG-I like helicases, RIG-I or Mda5, which transmit the signal through a common mitochondria-associated adaptor, MAVS. Although major breakthroughs have recently been made, much remains unknown about the mechanisms that translate virus recognition into antiviral genes expression. Beside the reputed detrimental role, reactive oxygen species (ROS) act as modulators of cellular signaling and gene regulation. NADPH oxidase (NOX) enzymes are a main source of deliberate cellular ROS production. Here, we found that NOX2 and ROS are required for the host cell to trigger an efficient RIG-I-mediated IRF-3 activation and downstream antiviral IFNβ and IFIT1 gene expression. Additionally, we provide evidence that NOX2 is critical for the expression of the central mitochondria-associated adaptor MAVS. Taken together these data reveal a new facet to the regulation of the innate host defense against viruses through the identification of an unrecognized role of NOX2 and ROS. The understanding of the mechanisms allowing the host to mount a rapid and efficient innate immune response to RNA viruses has been the subject of intensive research in recent years. Major groundwork allowed the identification of key sensors of virus nucleic acids, including RIG-I and Mda5, which through association with the MAVS adaptor initiate the signaling cascade required for activation of the IRF-3 transcription factor and downstream antiviral genes. Mechanisms of activation and degradation of key signaling molecules allow a tight control of the intensity and duration of the response. Our knowledge of how redox processes regulate signaling cascades is a fast moving field of research. Particularly, the identification of non-phagocytic reactive oxygen species-producing NADPH oxidase (NOX) enzymes revealed new insights into their function in innate immunity. Our endeavor in characterizing the role of NOX in the antiviral response reveals a new facet to the overall picture of antiviral response regulation. Here, we demonstrate that NOX2 is essential for MAVS expression in airway epithelial cells, thereby controlling the capacity of the cell to mount an efficient innate antiviral response following recognition of viruses. The innate immune response is essential to the host defense against viruses, through restriction of virus replication and coordination of the adaptive immune response. Induction of antiviral genes is a tightly regulated process initiated mainly through sensing of invading virus nucleic acids in the cytoplasm by RIG-I like helicases, RIG-I or Mda5, which transmit the signal through a common mitochondria-associated adaptor, MAVS. Although major breakthroughs have recently been made, much remains unknown about the mechanisms that translate virus recognition into antiviral genes expression. Beside the reputed detrimental role, reactive oxygen species (ROS) act as modulators of cellular signaling and gene regulation. NADPH oxidase (NOX) enzymes are a main source of deliberate cellular ROS production. Here, we found that NOX2 and ROS are required for the host cell to trigger an efficient RIG-I-mediated IRF-3 activation and downstream antiviral IFNbeta and IFIT1 gene expression. Additionally, we provide evidence that NOX2 is critical for the expression of the central mitochondria-associated adaptor MAVS. Taken together these data reveal a new facet to the regulation of the innate host defense against viruses through the identification of an unrecognized role of NOX2 and ROS. The innate immune response is essential to the host defense against viruses, through restriction of virus replication and coordination of the adaptive immune response. Induction of antiviral genes is a tightly regulated process initiated mainly through sensing of invading virus nucleic acids in the cytoplasm by RIG-I like helicases, RIG-I or Mda5, which transmit the signal through a common mitochondria-associated adaptor, MAVS. Although major breakthroughs have recently been made, much remains unknown about the mechanisms that translate virus recognition into antiviral genes expression. Beside the reputed detrimental role, reactive oxygen species (ROS) act as modulators of cellular signaling and gene regulation. NADPH oxidase (NOX) enzymes are a main source of deliberate cellular ROS production. Here, we found that NOX2 and ROS are required for the host cell to trigger an efficient RIG-I-mediated IRF-3 activation and downstream antiviral IFNβ and IFIT1 gene expression. Additionally, we provide evidence that NOX2 is critical for the expression of the central mitochondria-associated adaptor MAVS. Taken together these data reveal a new facet to the regulation of the innate host defense against viruses through the identification of an unrecognized role of NOX2 and ROS. The innate immune response is essential to the host defense against viruses, through restriction of virus replication and coordination of the adaptive immune response. Induction of antiviral genes is a tightly regulated process initiated mainly through sensing of invading virus nucleic acids in the cytoplasm by RIG-I like helicases, RIG-I or Mda5, which transmit the signal through a common mitochondria-associated adaptor, MAVS. Although major breakthroughs have recently been made, much remains unknown about the mechanisms that translate virus recognition into antiviral genes expression. Beside the reputed detrimental role, reactive oxygen species (ROS) act as modulators of cellular signaling and gene regulation. NADPH oxidase (NOX) enzymes are a main source of deliberate cellular ROS production. Here, we found that NOX2 and ROS are required for the host cell to trigger an efficient RIG-I-mediated IRF-3 activation and downstream antiviral IFNb and IFIT1 gene expression. Additionally, we provide evidence that NOX2 is critical for the expression of the central mitochondria-associated adaptor MAVS. Taken together these data reveal a new facet to the regulation of the innate host defense against viruses through the identification of an unrecognized role of NOX2 and ROS. The understanding of the mechanisms allowing the host to mount a rapid and efficient innate immune response to RNA viruses has been the subject of intensive research in recent years. Major groundwork allowed the identification of key sensors of virus nucleic acids, including RIG-I and Mda5, which through association with the MAVS adaptor initiate the signaling cascade required for activation of the IRF-3 transcription factor and downstream antiviral genes. Mechanisms of activation and degradation of key signaling molecules allow a tight control of the intensity and duration of the response. Our knowledge of how redox processes regulate signaling cascades is a fast moving field of research. Particularly, the identification of non-phagocytic reactive oxygen species-producing NADPH oxidase (NOX) enzymes revealed new insights into their function in innate immunity. Our endeavor in characterizing the role of NOX in the antiviral response reveals a new facet to the overall picture of antiviral response regulation. Here, we demonstrate that NOX2 is essential for MAVS expression in airway epithelial cells, thereby controlling the capacity of the cell to mount an efficient innate antiviral response following recognition of viruses. |
| Audience | Academic |
| Author | Jouan, Loubna Soucy-Faulkner, Anton Fink, Karin Vande Velde, Christine Nzengue, Yves Grandvaux, Nathalie Mukawera, Espérance Martel, Alexis Lamarre, Daniel |
| AuthorAffiliation | 1 CRCHUM - Centre Hospitalier de l'Université de Montréal, Montréal, Québec, Canada 2 Department of Biochemistry, Faculty of Medicine, Université de Montréal, Montréal, Québec, Canada North Carolina State University, United States of America 3 Department of Medicine, Faculty of Medicine, Université de Montréal, Montréal, Québec, Canada |
| AuthorAffiliation_xml | – name: North Carolina State University, United States of America – name: 1 CRCHUM - Centre Hospitalier de l'Université de Montréal, Montréal, Québec, Canada – name: 3 Department of Medicine, Faculty of Medicine, Université de Montréal, Montréal, Québec, Canada – name: 2 Department of Biochemistry, Faculty of Medicine, Université de Montréal, Montréal, Québec, Canada |
| Author_xml | – sequence: 1 givenname: Anton surname: Soucy-Faulkner fullname: Soucy-Faulkner, Anton – sequence: 2 givenname: Espérance surname: Mukawera fullname: Mukawera, Espérance – sequence: 3 givenname: Karin surname: Fink fullname: Fink, Karin – sequence: 4 givenname: Alexis surname: Martel fullname: Martel, Alexis – sequence: 5 givenname: Loubna surname: Jouan fullname: Jouan, Loubna – sequence: 6 givenname: Yves surname: Nzengue fullname: Nzengue, Yves – sequence: 7 givenname: Daniel surname: Lamarre fullname: Lamarre, Daniel – sequence: 8 givenname: Christine surname: Vande Velde fullname: Vande Velde, Christine – sequence: 9 givenname: Nathalie surname: Grandvaux fullname: Grandvaux, Nathalie |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20532218$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | COPYRIGHT 2010 Public Library of Science Soucy-Faulkner et al. 2010 2010 Soucy-Faulkner et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Soucy-Faulkner A, Mukawera E, Fink K, Martel A, Jouan L, et al. (2010) Requirement of NOX2 and Reactive Oxygen Species for Efficient RIG-I-Mediated Antiviral Response through Regulation of MAVS Expression. PLoS Pathog 6(6): e1000930. doi:10.1371/journal.ppat.1000930 |
| Copyright_xml | – notice: COPYRIGHT 2010 Public Library of Science – notice: Soucy-Faulkner et al. 2010 – notice: 2010 Soucy-Faulkner et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Soucy-Faulkner A, Mukawera E, Fink K, Martel A, Jouan L, et al. (2010) Requirement of NOX2 and Reactive Oxygen Species for Efficient RIG-I-Mediated Antiviral Response through Regulation of MAVS Expression. PLoS Pathog 6(6): e1000930. doi:10.1371/journal.ppat.1000930 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 Conceived and designed the experiments: ASF NG. Performed the experiments: ASF EM KF AM LJ YN CVV NG. Analyzed the data: ASF KF CVV NG. Contributed reagents/materials/analysis tools: DL. Wrote the paper: ASF NG. Supervised Loubna Jouan: DL. |
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| Snippet | The innate immune response is essential to the host defense against viruses, through restriction of virus replication and coordination of the adaptive immune... The innate immune response is essential to the host defense against viruses, through restriction of virus replication and coordination of the adaptive immune... |
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| SubjectTerms | adaptor proteins Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism Antimicrobial peptides Apoptosis Blotting, Western Bronchi - cytology Bronchi - immunology Bronchi - metabolism Carrier Proteins - genetics Carrier Proteins - metabolism Cell Biology/Cell Signaling Cells, Cultured CYBB protein Cytoplasm Data processing DEAD Box Protein 58 DEAD-box RNA Helicases - genetics DEAD-box RNA Helicases - metabolism DNA helicase Enzymes Epithelial cells Experiments Gene expression Gene Expression Regulation Gene regulation Humans Immune response Immune system Immunity Immunity, Innate Immunology/Innate Immunity Infectious Diseases/Viral Infections Interferon regulatory factor 3 Interferon Regulatory Factor-3 - genetics Interferon Regulatory Factor-3 - metabolism Interleukin-6 - genetics Interleukin-6 - metabolism Kinases Luciferases - metabolism Lung Neoplasms - immunology Lung Neoplasms - metabolism Lung Neoplasms - virology Medical research Membrane Glycoproteins - genetics Membrane Glycoproteins - metabolism Mitochondria Molecular Biology/Translational Regulation NAD(P)H oxidase NADPH Oxidase 2 NADPH Oxidases - genetics NADPH Oxidases - metabolism nucleic acids Oxidases Pathogens Physiological aspects Proteins Reactive oxygen species Reactive Oxygen Species - metabolism Receptors, Immunologic Replication Respiratory tract Respirovirus Infections - immunology Respirovirus Infections - metabolism Respirovirus Infections - virology Reverse Transcriptase Polymerase Chain Reaction RNA viruses RNA, Messenger - genetics RNA-Binding Proteins Sendai virus - physiology Signal Transduction Transcription Transcription factors Viruses |
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| Title | Requirement of NOX2 and Reactive Oxygen Species for Efficient RIG-I-Mediated Antiviral Response through Regulation of MAVS Expression |
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