Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections
Identifieur interne : 004521 ( Main/Merge ); précédent : 004520; suivant : 004522Cytokine 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.
- 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.
- 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
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<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>
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<term>Virus Diseases (virology)</term>
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<term>Cytokines (métabolisme)</term>
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<term>Infections de l'appareil respiratoire (immunologie)</term>
<term>Infections de l'appareil respiratoire (virologie)</term>
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<term>Interférons (métabolisme)</term>
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<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>
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<term>Interferons</term>
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<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>
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<author><name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name>
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</author>
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</author>
<author><name sortKey="Indoh, Tomokazu" sort="Indoh, Tomokazu" uniqKey="Indoh T" first="Tomokazu" last="Indoh">Tomokazu Indoh</name>
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</affiliation>
</author>
<author><name sortKey="Yokosawa, Noriko" sort="Yokosawa, Noriko" uniqKey="Yokosawa N" first="Noriko" last="Yokosawa">Noriko Yokosawa</name>
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</affiliation>
</author>
<author><name sortKey="Takashima, Ikuo" sort="Takashima, Ikuo" uniqKey="Takashima I" first="Ikuo" last="Takashima">Ikuo Takashima</name>
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</author>
<author><name sortKey="Tsutsumi, Hiroyuki" sort="Tsutsumi, Hiroyuki" uniqKey="Tsutsumi H" first="Hiroyuki" last="Tsutsumi">Hiroyuki Tsutsumi</name>
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</affiliation>
</author>
<author><name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name>
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<series><title level="j" type="main">Journal of Medical Virology</title>
<title level="j" type="alt">JOURNAL OF MEDICAL VIROLOGY</title>
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<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>
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<term>Induction levels</term>
<term>Infection</term>
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<term>Irf7</term>
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<term>Less induction</term>
<term>Many viruses</term>
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<term>Pathway</term>
<term>Post infection</term>
<term>Protein level</term>
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<term>Respiratory syncytial virus</term>
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<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>
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<author><name sortKey="Kariwa, Hiroaki" sort="Kariwa, Hiroaki" uniqKey="Kariwa H" first="Hiroaki" last="Kariwa">Hiroaki Kariwa</name>
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<author><name sortKey="Yokota, Shin Ichi" sort="Yokota, Shin Ichi" uniqKey="Yokota S" first="Shin-Ichi" last="Yokota">Shin-Ichi Yokota</name>
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<author><name sortKey="Iki, Shigeo" sort="Iki, Shigeo" uniqKey="Iki S" first="Shigeo" last="Iki">Shigeo Iki</name>
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<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 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>
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<author><name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name>
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<author><name sortKey="Kariwa, Hiroaki" sort="Kariwa, Hiroaki" uniqKey="Kariwa H" first="Hiroaki" last="Kariwa">Hiroaki Kariwa</name>
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<author><name sortKey="Yokota, Shin Ichi" sort="Yokota, Shin Ichi" uniqKey="Yokota S" first="Shin-Ichi" last="Yokota">Shin-Ichi Yokota</name>
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<author><name sortKey="Iki, Shigeo" sort="Iki, Shigeo" uniqKey="Iki S" first="Shigeo" last="Iki">Shigeo Iki</name>
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<author><name sortKey="Indoh, Tomokazu" sort="Indoh, Tomokazu" uniqKey="Indoh T" first="Tomokazu" last="Indoh">Tomokazu Indoh</name>
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<author><name sortKey="Yokosawa, Noriko" sort="Yokosawa, Noriko" uniqKey="Yokosawa N" first="Noriko" last="Yokosawa">Noriko Yokosawa</name>
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<term>Maladies virales (virologie)</term>
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<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>
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