Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections.
Identifieur interne : 002341 ( PubMed/Corpus ); précédent : 002340; suivant : 002342Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections.
Auteurs : Tamaki Okabayashi ; Hiroaki Kariwa ; Shin-Ichi Yokota ; Shigeo Iki ; Tomokazu Indoh ; Noriko Yokosawa ; Ikuo Takashima ; Hiroyuki Tsutsumi ; Nobuhiro FujiiSource :
- Journal of medical virology [ 0146-6615 ] ; 2006.
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
Links to Exploration step
pubmed:16482545Le document en format XML
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first="Tomokazu" last="Indoh">Tomokazu Indoh</name></author><author><name sortKey="Yokosawa, Noriko" sort="Yokosawa, Noriko" uniqKey="Yokosawa N" first="Noriko" last="Yokosawa">Noriko Yokosawa</name></author><author><name sortKey="Takashima, Ikuo" sort="Takashima, Ikuo" uniqKey="Takashima I" first="Ikuo" last="Takashima">Ikuo Takashima</name></author><author><name sortKey="Tsutsumi, Hiroyuki" sort="Tsutsumi, Hiroyuki" uniqKey="Tsutsumi H" first="Hiroyuki" last="Tsutsumi">Hiroyuki Tsutsumi</name></author><author><name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2006">2006</date><idno type="RBID">pubmed:16482545</idno><idno type="pmid">16482545</idno><idno type="doi">10.1002/jmv.20556</idno><idno type="wicri:Area/PubMed/Corpus">002341</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" 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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 Yokosawa</name></author><author><name sortKey="Takashima, Ikuo" sort="Takashima, Ikuo" uniqKey="Takashima I" first="Ikuo" last="Takashima">Ikuo Takashima</name></author><author><name sortKey="Tsutsumi, Hiroyuki" sort="Tsutsumi, Hiroyuki" uniqKey="Tsutsumi H" first="Hiroyuki" last="Tsutsumi">Hiroyuki Tsutsumi</name></author><author><name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name></author></analytic><series><title level="j">Journal of medical virology</title><idno type="ISSN">0146-6615</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Caco-2 Cells</term><term>Cell Line, Tumor</term><term>Cytokines (genetics)</term><term>Cytokines (metabolism)</term><term>Gene Expression Profiling</term><term>Humans</term><term>Interferons (genetics)</term><term>Interferons (metabolism)</term><term>Respiratory Tract Infections (immunology)</term><term>Respiratory Tract Infections (virology)</term><term>SARS Virus (pathogenicity)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Virus Diseases (immunology)</term><term>Virus Diseases (virology)</term><term>Virus Replication</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cytokines</term><term>Interferons</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Interferons</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Respiratory Tract Infections</term><term>Severe Acute Respiratory Syndrome</term><term>Virus Diseases</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Respiratory Tract Infections</term><term>Severe Acute Respiratory Syndrome</term><term>Virus Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Caco-2 Cells</term><term>Cell Line, Tumor</term><term>Gene Expression Profiling</term><term>Humans</term><term>Virus Replication</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 UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>9008-11-1</RegistryNumber><NameOfSubstance UI="D007372">Interferons</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D018938" MajorTopicYN="N">Caco-2 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007372" MajorTopicYN="N">Interferons</DescriptorName><QualifierName 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></record>Pour manipuler ce document sous Unix (Dilib)
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