Inhibition of cytokine gene expression and induction of chemokine genes in non-lymphatic cells infected with SARS coronavirus
Identifieur interne : 003E44 ( Main/Exploration ); précédent : 003E43; suivant : 003E45Inhibition of cytokine gene expression and induction of chemokine genes in non-lymphatic cells infected with SARS coronavirus
Auteurs : Martin Spiegel ; Friedemann WeberSource :
- Virology Journal [ 1743-422X ] ; 2006.
Descripteurs français
- KwdFr :
- ARN messager (génétique), ARN messager (métabolisme), Chimiokines (génétique), Cytokines (génétique), Extinction de l'expression des gènes, Humains, Lignée cellulaire, Rein (métabolisme), Rein (virologie), Régulation négative (génétique), Régulation positive (génétique), Transcription génétique, Tumeurs du côlon (génétique), Tumeurs du côlon (virologie), Virus du SRAS (physiologie).
- MESH :
- génétique : ARN messager, Chimiokines, Cytokines, Régulation négative, Régulation positive, Tumeurs du côlon.
- métabolisme : ARN messager, Rein.
- physiologie : Virus du SRAS.
- virologie : Rein, Tumeurs du côlon.
- Extinction de l'expression des gènes, Humains, Lignée cellulaire, Transcription génétique.
English descriptors
- KwdEn :
- Cell Line, Chemokines (genetics), Colonic Neoplasms (genetics), Colonic Neoplasms (virology), Cytokines (genetics), Down-Regulation (genetics), Gene Silencing, Humans, Kidney (metabolism), Kidney (virology), RNA, Messenger (genetics), RNA, Messenger (metabolism), SARS Virus (physiology), Transcription, Genetic, Up-Regulation (genetics).
- MESH :
- chemical , genetics : Chemokines, Cytokines, RNA, Messenger.
- genetics : Colonic Neoplasms, Down-Regulation, Up-Regulation.
- metabolism : Kidney, RNA, Messenger.
- physiology : SARS Virus.
- virology : Colonic Neoplasms, Kidney.
- Cell Line, Gene Silencing, Humans, Transcription, Genetic.
Abstract
SARS coronavirus (SARS-CoV) is the etiologic agent of the severe acute respiratory syndrome. SARS-CoV mainly infects tissues of non-lymphatic origin, and the cytokine profile of those cells can determine the course of disease. Here, we investigated the cytokine response of two human non-lymphatic cell lines, Caco-2 and HEK 293, which are fully permissive for SARS-CoV.
A comparison with established cytokine-inducing viruses revealed that SARS-CoV only weakly triggered a cytokine response. In particular, SARS-CoV did not activate significant transcription of the interferons IFN-α, IFN-β, IFN-λ1, IFN-λ2/3, as well as of the interferon-induced antiviral genes ISG56 and MxA, the chemokine RANTES and the interleukine IL-6. Interestingly, however, SARS-CoV strongly induced the chemokines IP-10 and IL-8 in the colon carcinoma cell line Caco-2, but not in the embryonic kidney cell line 293.
Our data indicate that SARS-CoV suppresses the antiviral cytokine system of non-immune cells to a large extent, thus buying time for dissemination in the host. However, synthesis of IP-10 and IL-8, which are established markers for acute-stage SARS, escapes the virus-induced silencing at least in some cell types. Therefore, the progressive infiltration of immune cells into the infected lungs observed in SARS patients could be due to the production of these chemokines by the infected tissue cells.
The online version of this article (doi:10.1186/1743-422X-3-17) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1186/1743-422X-3-17
PubMed: 16571117
PubMed Central: 1444920
Affiliations:
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Le document en format XML
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Germany</wicri:noCountry></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">16571117</idno><idno type="pmc">1444920</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1444920</idno><idno type="RBID">PMC:1444920</idno><idno type="doi">10.1186/1743-422X-3-17</idno><date when="2006">2006</date><idno type="wicri:Area/Pmc/Corpus">000491</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000491</idno><idno type="wicri:Area/Pmc/Curation">000491</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000491</idno><idno type="wicri:Area/Pmc/Checkpoint">001106</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">001106</idno><idno type="wicri:source">PubMed</idno><idno type="RBID">pubmed:16571117</idno><idno type="wicri:Area/PubMed/Corpus">002296</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" 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Spiegel</name><affiliation><nlm:aff id="Aff1">Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität, Freiburg, Freiburg D-79008 Germany</nlm:aff><wicri:noCountry code="subfield">Freiburg D-79008 Germany</wicri:noCountry></affiliation></author><author><name sortKey="Weber, Friedemann" sort="Weber, Friedemann" uniqKey="Weber F" first="Friedemann" last="Weber">Friedemann Weber</name><affiliation><nlm:aff id="Aff1">Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität, Freiburg, Freiburg D-79008 Germany</nlm:aff><wicri:noCountry code="subfield">Freiburg D-79008 Germany</wicri:noCountry></affiliation></author></analytic><series><title level="j">Virology Journal</title><idno type="eISSN">1743-422X</idno><imprint><date when="2006">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Line</term><term>Chemokines (genetics)</term><term>Colonic Neoplasms (genetics)</term><term>Colonic Neoplasms (virology)</term><term>Cytokines (genetics)</term><term>Down-Regulation (genetics)</term><term>Gene Silencing</term><term>Humans</term><term>Kidney (metabolism)</term><term>Kidney (virology)</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term><term>SARS Virus (physiology)</term><term>Transcription, Genetic</term><term>Up-Regulation (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term><term>ARN messager (métabolisme)</term><term>Chimiokines (génétique)</term><term>Cytokines (génétique)</term><term>Extinction de l'expression des gènes</term><term>Humains</term><term>Lignée cellulaire</term><term>Rein (métabolisme)</term><term>Rein (virologie)</term><term>Régulation négative (génétique)</term><term>Régulation positive (génétique)</term><term>Transcription génétique</term><term>Tumeurs du côlon (génétique)</term><term>Tumeurs du côlon (virologie)</term><term>Virus du SRAS (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Chemokines</term><term>Cytokines</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Colonic Neoplasms</term><term>Down-Regulation</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term><term>Chimiokines</term><term>Cytokines</term><term>Régulation négative</term><term>Régulation positive</term><term>Tumeurs du côlon</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Kidney</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Rein</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Rein</term><term>Tumeurs du côlon</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Colonic Neoplasms</term><term>Kidney</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Gene Silencing</term><term>Humans</term><term>Transcription, Genetic</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Extinction de l'expression des gènes</term><term>Humains</term><term>Lignée cellulaire</term><term>Transcription génétique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p>SARS coronavirus (SARS-CoV) is the etiologic agent of the severe acute respiratory syndrome. SARS-CoV mainly infects tissues of non-lymphatic origin, and the cytokine profile of those cells can determine the course of disease. Here, we investigated the cytokine response of two human non-lymphatic cell lines, Caco-2 and HEK 293, which are fully permissive for SARS-CoV.</p></sec><sec><title>Results</title><p>A comparison with established cytokine-inducing viruses revealed that SARS-CoV only weakly triggered a cytokine response. In particular, SARS-CoV did not activate significant transcription of the interferons IFN-α, IFN-β, IFN-λ1, IFN-λ2/3, as well as of the interferon-induced antiviral genes ISG56 and MxA, the chemokine RANTES and the interleukine IL-6. Interestingly, however, SARS-CoV strongly induced the chemokines IP-10 and IL-8 in the colon carcinoma cell line Caco-2, but not in the embryonic kidney cell line 293.</p></sec><sec><title>Conclusion</title><p>Our data indicate that SARS-CoV suppresses the antiviral cytokine system of non-immune cells to a large extent, thus buying time for dissemination in the host. However, synthesis of IP-10 and IL-8, which are established markers for acute-stage SARS, escapes the virus-induced silencing at least in some cell types. Therefore, the progressive infiltration of immune cells into the infected lungs observed in SARS patients could be due to the production of these chemokines by the infected tissue cells.</p></sec><sec><title>Electronic supplementary material</title><p>The online version of this article (doi:10.1186/1743-422X-3-17) contains supplementary material, which is available to authorized users.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Samuel, Ce" uniqKey="Samuel C">CE Samuel</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rollins, Bj" uniqKey="Rollins B">BJ Rollins</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Weber, F" uniqKey="Weber F">F Weber</name></author><author><name sortKey="Kochs, G" uniqKey="Kochs G">G Kochs</name></author><author><name sortKey="Haller, O" uniqKey="Haller O">O 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U">U Stroher</name></author><author><name sortKey="Dicaro, A" uniqKey="Dicaro A">A DiCaro</name></author><author><name sortKey="Li, Y" uniqKey="Li Y">Y Li</name></author><author><name sortKey="Strong, Je" uniqKey="Strong J">JE Strong</name></author><author><name sortKey="Aoki, F" uniqKey="Aoki F">F Aoki</name></author><author><name sortKey="Plummer, F" uniqKey="Plummer F">F Plummer</name></author><author><name sortKey="Jones, Sm" uniqKey="Jones S">SM Jones</name></author><author><name sortKey="Feldmann, H" uniqKey="Feldmann H">H Feldmann</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list></list><tree><noCountry><name sortKey="Spiegel, Martin" sort="Spiegel, Martin" uniqKey="Spiegel M" first="Martin" last="Spiegel">Martin Spiegel</name><name sortKey="Weber, Friedemann" sort="Weber, Friedemann" uniqKey="Weber F" first="Friedemann" last="Weber">Friedemann Weber</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix 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