IL-17 boosts proinflammatory outcome of antiviral response in human cells.
Identifieur interne : 001465 ( PubMed/Curation ); précédent : 001464; suivant : 001466IL-17 boosts proinflammatory outcome of antiviral response in human cells.
Auteurs : Grigory Ryzhakov [Royaume-Uni] ; Cheryl Chuk-Ke Lai ; Katrina Blazek ; Ken-Win To ; Tracy Hussell ; Irina UdalovaSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2011.
Descripteurs français
- KwdFr :
- Antiviraux (métabolisme), Antiviraux (pharmacologie), Cellules cultivées, Cytokines (antagonistes et inhibiteurs), Cytokines (biosynthèse), Cytokines (physiologie), Facteur de transcription RelA (biosynthèse), Facteur de transcription RelA (génétique), Facteur de transcription RelA (physiologie), Facteur-3 de régulation d'interféron (biosynthèse), Facteur-3 de régulation d'interféron (génétique), Facteur-3 de régulation d'interféron (physiologie), Fibroblastes (anatomopathologie), Fibroblastes (immunologie), Fibroblastes (virologie), Humains, I-kappa B Kinase (biosynthèse), I-kappa B Kinase (génétique), I-kappa B Kinase (physiologie), Interleukine-17 (physiologie), Médiateurs de l'inflammation (métabolisme), Médiateurs de l'inflammation (physiologie), Peau (anatomopathologie), Peau (immunologie), Peau (virologie), Poly I-C (antagonistes et inhibiteurs), Poly I-C (pharmacologie), Régulation de l'expression des gènes (immunologie), Régulation positive (immunologie), Transduction du signal (génétique), Transduction du signal (immunologie), Virus respiratoires syncytiaux (immunologie).
- MESH :
- anatomopathologie : Fibroblastes, Peau.
- antagonistes et inhibiteurs : Cytokines, Poly I-C.
- biosynthèse : Cytokines, Facteur de transcription RelA, Facteur-3 de régulation d'interféron, I-kappa B Kinase.
- génétique : Facteur de transcription RelA, Facteur-3 de régulation d'interféron, I-kappa B Kinase, Transduction du signal.
- immunologie : Fibroblastes, Peau, Régulation de l'expression des gènes, Régulation positive, Transduction du signal, Virus respiratoires syncytiaux.
- métabolisme : Antiviraux, Médiateurs de l'inflammation.
- pharmacologie : Antiviraux, Poly I-C.
- physiologie : Cytokines, Facteur de transcription RelA, Facteur-3 de régulation d'interféron, I-kappa B Kinase, Interleukine-17, Médiateurs de l'inflammation.
- virologie : Fibroblastes, Peau.
- Cellules cultivées, Humains.
English descriptors
- KwdEn :
- Antiviral Agents (metabolism), Antiviral Agents (pharmacology), Cells, Cultured, Cytokines (antagonists & inhibitors), Cytokines (biosynthesis), Cytokines (physiology), Fibroblasts (immunology), Fibroblasts (pathology), Fibroblasts (virology), Gene Expression Regulation (immunology), Humans, I-kappa B Kinase (biosynthesis), I-kappa B Kinase (genetics), I-kappa B Kinase (physiology), Inflammation Mediators (metabolism), Inflammation Mediators (physiology), Interferon Regulatory Factor-3 (biosynthesis), Interferon Regulatory Factor-3 (genetics), Interferon Regulatory Factor-3 (physiology), Interleukin-17 (physiology), Poly I-C (antagonists & inhibitors), Poly I-C (pharmacology), Respiratory Syncytial Viruses (immunology), Signal Transduction (genetics), Signal Transduction (immunology), Skin (immunology), Skin (pathology), Skin (virology), Transcription Factor RelA (biosynthesis), Transcription Factor RelA (genetics), Transcription Factor RelA (physiology), Up-Regulation (immunology).
- MESH :
- chemical , antagonists & inhibitors : Cytokines, Poly I-C.
- chemical , biosynthesis : Cytokines, I-kappa B Kinase, Interferon Regulatory Factor-3, Transcription Factor RelA.
- chemical , genetics : I-kappa B Kinase, Interferon Regulatory Factor-3, Transcription Factor RelA.
- chemical , metabolism : Antiviral Agents, Inflammation Mediators.
- chemical , pharmacology : Antiviral Agents, Poly I-C.
- chemical , physiology : Cytokines, I-kappa B Kinase, Inflammation Mediators, Interferon Regulatory Factor-3, Interleukin-17, Transcription Factor RelA.
- genetics : Signal Transduction.
- immunology : Fibroblasts, Gene Expression Regulation, Respiratory Syncytial Viruses, Signal Transduction, Skin, Up-Regulation.
- pathology : Fibroblasts, Skin.
- virology : Fibroblasts, Skin.
- Cells, Cultured, Humans.
Abstract
Excessive inflammation during bacterial and viral infections is destructive to the host and involves elevated production of proinflammatory cytokines. It is especially deleterious in organs with space constraints such as lung and the CNS. Indeed, a number of viruses that infect lungs, such as avian influenza virus, SARS-associated coronavirus, and respiratory syncytial virus, elicit a very high level of proinflammatory cytokines; however, it is unclear what triggers their production. In this study, we show that IL-17 commonly produced during viral infection specifically augments a proinflammatory response by directly synergizing with antiviral signaling. Costimulation of primary human fibroblasts with IL-17 greatly enhanced respiratory syncytial virus-induced or synthetic dsRNA-based viral mimic polyinosinic:polycytidylic acid-induced expression of proinflammatory genes without affecting expression of IFN-β-stimulated or IFN-stimulated genes. Knockdown of expression of known mediators of the antiviral signaling pathway revealed that the IL-17-poly(I:C) synergy depends on the presence of the transcriptional factors RelA and IFN regulatory factor 3 and IκB kinases. Moreover, this synergy was blocked by an IκB kinase inhibitor, BAY 11-7082. These findings shed light on the molecular mechanisms behind IL-17-dependent immunopathology observed in viral infections.
DOI: 10.4049/jimmunol.1100917
PubMed: 21964025
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(pathology)</term><term>Skin (virology)</term><term>Transcription Factor RelA (biosynthesis)</term><term>Transcription Factor RelA (genetics)</term><term>Transcription Factor RelA (physiology)</term><term>Up-Regulation (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antiviraux (métabolisme)</term><term>Antiviraux (pharmacologie)</term><term>Cellules cultivées</term><term>Cytokines (antagonistes et inhibiteurs)</term><term>Cytokines (biosynthèse)</term><term>Cytokines (physiologie)</term><term>Facteur de transcription RelA (biosynthèse)</term><term>Facteur de transcription RelA (génétique)</term><term>Facteur de transcription RelA (physiologie)</term><term>Facteur-3 de régulation d'interféron (biosynthèse)</term><term>Facteur-3 de régulation d'interféron (génétique)</term><term>Facteur-3 de régulation d'interféron (physiologie)</term><term>Fibroblastes (anatomopathologie)</term><term>Fibroblastes (immunologie)</term><term>Fibroblastes 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xml:lang="fr"><term>Fibroblastes</term><term>Peau</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Fibroblasts</term><term>Skin</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cells, Cultured</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules cultivées</term><term>Humains</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Excessive inflammation during bacterial and viral infections is destructive to the host and involves elevated production of proinflammatory cytokines. It is especially deleterious in organs with space constraints such as lung and the CNS. Indeed, a number of viruses that infect lungs, such as avian influenza virus, SARS-associated coronavirus, and respiratory syncytial virus, elicit a very high level of proinflammatory cytokines; however, it is unclear what triggers their production. In this study, we show that IL-17 commonly produced during viral infection specifically augments a proinflammatory response by directly synergizing with antiviral signaling. Costimulation of primary human fibroblasts with IL-17 greatly enhanced respiratory syncytial virus-induced or synthetic dsRNA-based viral mimic polyinosinic:polycytidylic acid-induced expression of proinflammatory genes without affecting expression of IFN-β-stimulated or IFN-stimulated genes. Knockdown of expression of known mediators of the antiviral signaling pathway revealed that the IL-17-poly(I:C) synergy depends on the presence of the transcriptional factors RelA and IFN regulatory factor 3 and IκB kinases. Moreover, this synergy was blocked by an IκB kinase inhibitor, BAY 11-7082. These findings shed light on the molecular mechanisms behind IL-17-dependent immunopathology observed in viral infections.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21964025</PMID><DateCompleted><Year>2012</Year><Month>01</Month><Day>09</Day></DateCompleted><DateRevised><Year>2017</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1550-6606</ISSN><JournalIssue CitedMedium="Internet"><Volume>187</Volume><Issue>10</Issue><PubDate><Year>2011</Year><Month>Nov</Month><Day>15</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J. Immunol.</ISOAbbreviation></Journal><ArticleTitle>IL-17 boosts proinflammatory outcome of antiviral response in human cells.</ArticleTitle><Pagination><MedlinePgn>5357-62</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4049/jimmunol.1100917</ELocationID><Abstract><AbstractText>Excessive inflammation during bacterial and viral infections is destructive to the host and involves elevated production of proinflammatory cytokines. It is especially deleterious in organs with space constraints such as lung and the CNS. Indeed, a number of viruses that infect lungs, such as avian influenza virus, SARS-associated coronavirus, and respiratory syncytial virus, elicit a very high level of proinflammatory cytokines; however, it is unclear what triggers their production. In this study, we show that IL-17 commonly produced during viral infection specifically augments a proinflammatory response by directly synergizing with antiviral signaling. Costimulation of primary human fibroblasts with IL-17 greatly enhanced respiratory syncytial virus-induced or synthetic dsRNA-based viral mimic polyinosinic:polycytidylic acid-induced expression of proinflammatory genes without affecting expression of IFN-β-stimulated or IFN-stimulated genes. Knockdown of expression of known mediators of the antiviral signaling pathway revealed that the IL-17-poly(I:C) synergy depends on the presence of the transcriptional factors RelA and IFN regulatory factor 3 and IκB kinases. Moreover, this synergy was blocked by an IκB kinase inhibitor, BAY 11-7082. These findings shed light on the molecular mechanisms behind IL-17-dependent immunopathology observed in viral infections.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ryzhakov</LastName><ForeName>Grigory</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Kennedy Institute of Rheumatology, University of Oxford, London W6 8LH, UK. grigory.ryzhakov@kennedy.ox.ac.uk</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lai</LastName><ForeName>Cheryl Chuk-ke</ForeName><Initials>CC</Initials></Author><Author ValidYN="Y"><LastName>Blazek</LastName><ForeName>Katrina</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>To</LastName><ForeName>Ken-win</ForeName><Initials>KW</Initials></Author><Author ValidYN="Y"><LastName>Hussell</LastName><ForeName>Tracy</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Udalova</LastName><ForeName>Irina</ForeName><Initials>I</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>G0802752</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><Agency>Arthritis Research UK</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>09</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Immunol</MedlineTA><NlmUniqueID>2985117R</NlmUniqueID><ISSNLinking>0022-1767</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000998">Antiviral Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494232">IRF3 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018836">Inflammation Mediators</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050838">Interferon Regulatory Factor-3</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020381">Interleukin-17</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C498143">RELA protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051996">Transcription Factor RelA</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.10</RegistryNumber><NameOfSubstance UI="D051550">I-kappa B Kinase</NameOfSubstance></Chemical><Chemical><RegistryNumber>O84C90HH2L</RegistryNumber><NameOfSubstance UI="D011070">Poly I-C</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000998" MajorTopicYN="N">Antiviral Agents</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005347" MajorTopicYN="N">Fibroblasts</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051550" MajorTopicYN="N">I-kappa B Kinase</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018836" MajorTopicYN="N">Inflammation Mediators</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050838" MajorTopicYN="N">Interferon Regulatory Factor-3</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020381" MajorTopicYN="N">Interleukin-17</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011070" MajorTopicYN="N">Poly I-C</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012136" MajorTopicYN="N">Respiratory Syncytial 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