Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections
Identifieur interne : 000126 ( Istex/Curation ); précédent : 000125; suivant : 000127Cytokine 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.
English descriptors
- Teeft :
- Ace2, Antiviral, Biochem biophys, Caco2, Caco2 cells, Cell lines, Chan, Clinical progression, Coronavirus, Culture medium, Cytokine, Cytokine production, Cytokine regulation, Distress syndrome, Fluav, Gapdh, Gapdh mrna, Hokkaido, Hpiv2, Hpiv2 infections, Human virus type, 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 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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first="Hiroaki" last="Kariwa">Hiroaki Kariwa</name><affiliation wicri:level="1"><mods:affiliation>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Hokkaido, Japan</mods:affiliation><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></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"><mods:affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, 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Hokkaido</wicri:regionArea></affiliation></author><author><name sortKey="Yokosawa, Noriko" sort="Yokosawa, Noriko" uniqKey="Yokosawa N" first="Noriko" last="Yokosawa">Noriko Yokosawa</name><affiliation wicri:level="1"><mods:affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido</wicri:regionArea></affiliation></author><author><name sortKey="Takashima, Ikuo" sort="Takashima, Ikuo" uniqKey="Takashima I" first="Ikuo" last="Takashima">Ikuo Takashima</name><affiliation wicri:level="1"><mods:affiliation>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Hokkaido, Japan</mods:affiliation><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></affiliation></author><author><name sortKey="Tsutsumi, Hiroyuki" sort="Tsutsumi, Hiroyuki" uniqKey="Tsutsumi H" first="Hiroyuki" last="Tsutsumi">Hiroyuki Tsutsumi</name><affiliation wicri:level="1"><mods:affiliation>Department of Pediatrics, Sapporo Medical University School of Medicine, Hokkaido, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pediatrics, Sapporo Medical University School of Medicine, Hokkaido</wicri:regionArea></affiliation></author><author><name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name><affiliation wicri:level="1"><mods:affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: fujii@sapmed.ac.jp</mods:affiliation><country wicri:rule="url">Japon</country></affiliation><affiliation wicri:level="1"><mods:affiliation>Correspondence address: Department of Microbiology, Sapporo Medical University School of Medicine, South‐1, West‐17, Chuo‐ku, Sapporo 060‐8556, Hokkaido, Japan.===</mods:affiliation><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></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="Teeft" xml:lang="en"><term>Ace2</term><term>Antiviral</term><term>Biochem biophys</term><term>Caco2</term><term>Caco2 cells</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>Hokkaido</term><term>Hpiv2</term><term>Hpiv2 infections</term><term>Human virus type</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 infection</term><term>Zhang</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></record>Pour manipuler ce document sous Unix (Dilib)
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