Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections.
Identifieur interne : 001381 ( Ncbi/Merge ); précédent : 001380; suivant : 001382Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections.
Auteurs : Tamaki Okabayashi [Japon] ; Hiroaki Kariwa ; Shin-Ichi Yokota ; Shigeo Iki ; Tomokazu Indoh ; Noriko Yokosawa ; Ikuo Takashima ; Hiroyuki Tsutsumi ; Nobuhiro FujiiSource :
- Journal of medical virology [ 0146-6615 ] ; 2006.
Descripteurs français
- KwdFr :
- Analyse de profil d'expression de gènes, Cellules Caco-2, Cytokines (génétique), Cytokines (métabolisme), Humains, Infections de l'appareil respiratoire (immunologie), Infections de l'appareil respiratoire (virologie), Interférons (génétique), Interférons (métabolisme), Lignée cellulaire tumorale, Maladies virales (immunologie), Maladies virales (virologie), Réplication virale, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (pathogénicité).
- MESH :
- génétique : Cytokines, Interférons.
- immunologie : Infections de l'appareil respiratoire, Maladies virales, Syndrome respiratoire aigu sévère.
- métabolisme : Cytokines, Interférons.
- pathogénicité : Virus du SRAS.
- virologie : Infections de l'appareil respiratoire, Maladies virales, Syndrome respiratoire aigu sévère.
- Analyse de profil d'expression de gènes, Cellules Caco-2, Humains, Lignée cellulaire tumorale, Réplication virale.
English descriptors
- KwdEn :
- Caco-2 Cells, Cell Line, Tumor, Cytokines (genetics), Cytokines (metabolism), Gene Expression Profiling, Humans, Interferons (genetics), Interferons (metabolism), Respiratory Tract Infections (immunology), Respiratory Tract Infections (virology), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology), Virus Diseases (immunology), Virus Diseases (virology), Virus Replication.
- MESH :
- chemical , genetics : Cytokines, Interferons.
- chemical , metabolism : Cytokines, Interferons.
- immunology : Respiratory Tract Infections, Severe Acute Respiratory Syndrome, Virus Diseases.
- pathogenicity : SARS Virus.
- virology : Respiratory Tract Infections, Severe Acute Respiratory Syndrome, Virus Diseases.
- Caco-2 Cells, Cell Line, Tumor, Gene Expression Profiling, Humans, Virus Replication.
Abstract
The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS.
DOI: 10.1002/jmv.20556
PubMed: 16482545
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Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido</wicri:regionArea><wicri:noRegion>Hokkaido</wicri:noRegion></affiliation></author><author><name sortKey="Kariwa, Hiroaki" sort="Kariwa, Hiroaki" uniqKey="Kariwa H" first="Hiroaki" last="Kariwa">Hiroaki Kariwa</name></author><author><name sortKey="Yokota, Shin Ichi" sort="Yokota, Shin Ichi" uniqKey="Yokota S" first="Shin-Ichi" last="Yokota">Shin-Ichi Yokota</name></author><author><name sortKey="Iki, Shigeo" sort="Iki, Shigeo" uniqKey="Iki S" first="Shigeo" last="Iki">Shigeo Iki</name></author><author><name sortKey="Indoh, Tomokazu" sort="Indoh, Tomokazu" uniqKey="Indoh T" first="Tomokazu" last="Indoh">Tomokazu Indoh</name></author><author><name sortKey="Yokosawa, Noriko" sort="Yokosawa, Noriko" uniqKey="Yokosawa N" first="Noriko" last="Yokosawa">Noriko 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cellulaire tumorale</term><term>Réplication virale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16482545</PMID><DateCompleted><Year>2006</Year><Month>05</Month><Day>26</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0146-6615</ISSN><JournalIssue CitedMedium="Print"><Volume>78</Volume><Issue>4</Issue><PubDate><Year>2006</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Journal of medical virology</Title><ISOAbbreviation>J. Med. Virol.</ISOAbbreviation></Journal><ArticleTitle>Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections.</ArticleTitle><Pagination><MedlinePgn>417-24</MedlinePgn></Pagination><Abstract><AbstractText>The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS.</AbstractText><CopyrightInformation>Copyright 2006 Wiley-Liss, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Okabayashi</LastName><ForeName>Tamaki</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kariwa</LastName><ForeName>Hiroaki</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Yokota</LastName><ForeName>Shin-ichi</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Iki</LastName><ForeName>Shigeo</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Indoh</LastName><ForeName>Tomokazu</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Yokosawa</LastName><ForeName>Noriko</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Takashima</LastName><ForeName>Ikuo</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Tsutsumi</LastName><ForeName>Hiroyuki</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Fujii</LastName><ForeName>Nobuhiro</ForeName><Initials>N</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Med Virol</MedlineTA><NlmUniqueID>7705876</NlmUniqueID><ISSNLinking>0146-6615</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012141" MajorTopicYN="N">Respiratory Tract Infections</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014777" MajorTopicYN="N">Virus Diseases</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>2</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>5</Month><Day>27</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>2</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16482545</ArticleId><ArticleId IdType="doi">10.1002/jmv.20556</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Japon</li></country></list><tree><noCountry><name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name><name sortKey="Iki, Shigeo" sort="Iki, Shigeo" uniqKey="Iki S" first="Shigeo" last="Iki">Shigeo Iki</name><name sortKey="Indoh, Tomokazu" sort="Indoh, Tomokazu" uniqKey="Indoh T" first="Tomokazu" last="Indoh">Tomokazu Indoh</name><name sortKey="Kariwa, Hiroaki" sort="Kariwa, Hiroaki" uniqKey="Kariwa H" first="Hiroaki" last="Kariwa">Hiroaki Kariwa</name><name sortKey="Takashima, Ikuo" sort="Takashima, Ikuo" uniqKey="Takashima I" first="Ikuo" last="Takashima">Ikuo Takashima</name><name sortKey="Tsutsumi, Hiroyuki" sort="Tsutsumi, Hiroyuki" uniqKey="Tsutsumi H" first="Hiroyuki" last="Tsutsumi">Hiroyuki Tsutsumi</name><name sortKey="Yokosawa, Noriko" sort="Yokosawa, Noriko" uniqKey="Yokosawa N" first="Noriko" last="Yokosawa">Noriko Yokosawa</name><name sortKey="Yokota, Shin Ichi" sort="Yokota, Shin Ichi" uniqKey="Yokota S" first="Shin-Ichi" last="Yokota">Shin-Ichi Yokota</name></noCountry><country name="Japon"><noRegion><name sortKey="Okabayashi, Tamaki" sort="Okabayashi, Tamaki" uniqKey="Okabayashi T" first="Tamaki" last="Okabayashi">Tamaki Okabayashi</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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