Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections
Identifieur interne : 004305 ( Main/Exploration ); précédent : 004304; suivant : 004306Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections
Auteurs : Tamaki Okabayashi [Japon] ; Hiroaki Kariwa [Japon] ; Shin-Ichi Yokota [Japon] ; Shigeo Iki [Japon] ; Tomokazu Indoh [Japon] ; Noriko Yokosawa [Japon] ; Ikuo Takashima [Japon] ; Hiroyuki Tsutsumi [Japon] ; Nobuhiro Fujii [Japon]Source :
- Journal of Medical Virology [ 0146-6615 ] ; 2006-04.
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.
- Pascal (Inist)
- MESH :
English descriptors
- KwdEn :
- Caco-2 Cells, Cell Line, Tumor, Cytokine, Cytokines (genetics), Cytokines (metabolism), Gene Expression Profiling, Humans, Interferons (genetics), Interferons (metabolism), Interleukin 6, Respiratory Tract Infections (immunology), Respiratory Tract Infections (virology), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology), Severe acute respiratory syndrome, Severe acute respiratory syndrome virus, Viral disease, 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.
- Teeft :
- Ace2, Antiviral, Biochem biophys, Caco-2 Cells, Caco2, Caco2 cells, Cell Line, Tumor, Cell lines, Chan, Clinical progression, Coronavirus, Culture medium, Cytokine, Cytokine production, Cytokine regulation, Distress syndrome, Fluav, Gapdh, Gapdh mrna, Gene Expression Profiling, Hokkaido, Hpiv2, Hpiv2 infections, Human virus type, Humans, Ifns, Important role, Induction, Induction levels, Infection, Interferon, Irf7, Isgs, Less induction, Many viruses, Mrna, Negative regulator, Pathway, Post infection, Protein level, Rantes, Receptor, Regulator, Replication, Respir crit care, Respiratory syncytial virus, Respiratory syndrome, Sars, Sars coronavirus, Sars patients, Signal transduction, Signal transduction pathway, Siha cells, Socs family, Socs3, Stat3, Syncytial, Syndrome, Transduction, University school, Viral, Virol, Virus, Virus Replication, Virus infection, Zhang.
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. J. Med. Virol. 78:417–424, 2006. © 2006 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jmv.20556
Affiliations:
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Okabayashi</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, 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><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Hokkaido</wicri:regionArea><wicri:noRegion>Hokkaido</wicri:noRegion></affiliation></author><author><name sortKey="Yokota, Shin Chi" sort="Yokota, Shin Chi" uniqKey="Yokota S" first="Shin-Ichi" last="Yokota">Shin-Ichi Yokota</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido</wicri:regionArea><wicri:noRegion>Hokkaido</wicri:noRegion></affiliation></author><author><name sortKey="Iki, Shigeo" sort="Iki, Shigeo" uniqKey="Iki S" first="Shigeo" last="Iki">Shigeo Iki</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido</wicri:regionArea><wicri:noRegion>Hokkaido</wicri:noRegion></affiliation></author><author><name sortKey="Indoh, Tomokazu" sort="Indoh, Tomokazu" uniqKey="Indoh T" first="Tomokazu" last="Indoh">Tomokazu Indoh</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido</wicri:regionArea><wicri:noRegion>Hokkaido</wicri:noRegion></affiliation></author><author><name sortKey="Yokosawa, Noriko" sort="Yokosawa, Noriko" uniqKey="Yokosawa N" first="Noriko" last="Yokosawa">Noriko Yokosawa</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido</wicri:regionArea><wicri:noRegion>Hokkaido</wicri:noRegion></affiliation></author><author><name sortKey="Takashima, Ikuo" sort="Takashima, Ikuo" uniqKey="Takashima I" first="Ikuo" last="Takashima">Ikuo Takashima</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Hokkaido</wicri:regionArea><wicri:noRegion>Hokkaido</wicri:noRegion></affiliation></author><author><name sortKey="Tsutsumi, Hiroyuki" sort="Tsutsumi, Hiroyuki" uniqKey="Tsutsumi H" first="Hiroyuki" last="Tsutsumi">Hiroyuki Tsutsumi</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pediatrics, Sapporo Medical University School of Medicine, Hokkaido</wicri:regionArea><wicri:noRegion>Hokkaido</wicri:noRegion></affiliation></author><author><name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido</wicri:regionArea><wicri:noRegion>Hokkaido</wicri:noRegion></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Japon</country></affiliation><affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">Japon</country><wicri:regionArea>Correspondence address: Department of Microbiology, Sapporo Medical University School of Medicine, South‐1, West‐17, Chuo‐ku, Sapporo 060‐8556, Hokkaido</wicri:regionArea><wicri:noRegion>Hokkaido</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Medical Virology</title><title level="j" type="alt">JOURNAL OF MEDICAL VIROLOGY</title><idno type="ISSN">0146-6615</idno><idno type="eISSN">1096-9071</idno><imprint><biblScope unit="vol">78</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="417">417</biblScope><biblScope unit="page" to="424">424</biblScope><biblScope unit="page-count">8</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-04">2006-04</date></imprint><idno type="ISSN">0146-6615</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0146-6615</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Caco-2 Cells</term><term>Cell Line, Tumor</term><term>Cytokine</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>Interleukin 6</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>Severe acute respiratory syndrome</term><term>Severe acute respiratory syndrome virus</term><term>Viral disease</term><term>Virus Diseases (immunology)</term><term>Virus Diseases (virology)</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Cellules Caco-2</term><term>Cytokines (génétique)</term><term>Cytokines (métabolisme)</term><term>Humains</term><term>Infections de l'appareil respiratoire (immunologie)</term><term>Infections de l'appareil respiratoire (virologie)</term><term>Interférons (génétique)</term><term>Interférons (métabolisme)</term><term>Lignée cellulaire tumorale</term><term>Maladies virales (immunologie)</term><term>Maladies virales (virologie)</term><term>Réplication virale</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Virus du SRAS (pathogénicité)</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="génétique" xml:lang="fr"><term>Cytokines</term><term>Interférons</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Infections de l'appareil respiratoire</term><term>Maladies virales</term><term>Syndrome respiratoire aigu sévère</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="métabolisme" xml:lang="fr"><term>Cytokines</term><term>Interférons</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections de l'appareil respiratoire</term><term>Maladies virales</term><term>Syndrome respiratoire aigu sévère</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="Pascal" xml:lang="fr"><term>Cytokine</term><term>Interleukine 6</term><term>Syndrome respiratoire aigu sévère</term><term>Virose</term><term>Virus syndrome respiratoire aigu sévère</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Ace2</term><term>Antiviral</term><term>Biochem biophys</term><term>Caco-2 Cells</term><term>Caco2</term><term>Caco2 cells</term><term>Cell Line, Tumor</term><term>Cell lines</term><term>Chan</term><term>Clinical progression</term><term>Coronavirus</term><term>Culture medium</term><term>Cytokine</term><term>Cytokine production</term><term>Cytokine regulation</term><term>Distress syndrome</term><term>Fluav</term><term>Gapdh</term><term>Gapdh mrna</term><term>Gene Expression Profiling</term><term>Hokkaido</term><term>Hpiv2</term><term>Hpiv2 infections</term><term>Human virus type</term><term>Humans</term><term>Ifns</term><term>Important role</term><term>Induction</term><term>Induction levels</term><term>Infection</term><term>Interferon</term><term>Irf7</term><term>Isgs</term><term>Less induction</term><term>Many viruses</term><term>Mrna</term><term>Negative regulator</term><term>Pathway</term><term>Post infection</term><term>Protein level</term><term>Rantes</term><term>Receptor</term><term>Regulator</term><term>Replication</term><term>Respir crit care</term><term>Respiratory syncytial virus</term><term>Respiratory syndrome</term><term>Sars</term><term>Sars coronavirus</term><term>Sars patients</term><term>Signal transduction</term><term>Signal transduction pathway</term><term>Siha cells</term><term>Socs family</term><term>Socs3</term><term>Stat3</term><term>Syncytial</term><term>Syndrome</term><term>Transduction</term><term>University school</term><term>Viral</term><term>Virol</term><term>Virus</term><term>Virus Replication</term><term>Virus infection</term><term>Zhang</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Cellules Caco-2</term><term>Humains</term><term>Lignée 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. J. Med. Virol. 78:417–424, 2006. © 2006 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Okabayashi, Tamaki" sort="Okabayashi, Tamaki" uniqKey="Okabayashi T" first="Tamaki" last="Okabayashi">Tamaki Okabayashi</name></noRegion><name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name><name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name><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 Chi" sort="Yokota, Shin Chi" uniqKey="Yokota S" first="Shin-Ichi" last="Yokota">Shin-Ichi Yokota</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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