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Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections

Identifieur interne : 000491 ( PascalFrancis/Curation ); précédent : 000490; suivant : 000492

Cytokine 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 :

RBID : Pascal:06-0257225

Descripteurs français

English descriptors

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.
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A11 04  1    @1 IKI (Shigeo)
A11 05  1    @1 INDOH (Tomokazu)
A11 06  1    @1 YOKOSAWA (Noriko)
A11 07  1    @1 TAKASHIMA (Ikuo)
A11 08  1    @1 TSUTSUMI (Hiroyuki)
A11 09  1    @1 FUJII (Nobuhiro)
A14 01      @1 Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku @2 Sapporo, Hokkaido @3 JPN @Z 1 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut. @Z 9 aut.
A14 02      @1 Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University @2 Hokkaido @3 JPN @Z 2 aut. @Z 7 aut.
A14 03      @1 Department of Pediatrics, Sapporo Medical University School of Medicine @2 Hokkaido @3 JPN @Z 8 aut.
A20       @1 417-424
A21       @1 2006
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C01 01    ENG  @0 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.
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C03 02  X  SPA  @0 Citoquina @5 05
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C03 03  X  SPA  @0 Interleuquina 6 @5 06
C03 04  X  FRE  @0 Virose @5 14
C03 04  X  ENG  @0 Viral disease @5 14
C03 04  X  SPA  @0 Virosis @5 14
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C07 03  X  FRE  @0 Nidovirales @2 NW
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C07 05  X  FRE  @0 Appareil respiratoire pathologie @5 13
C07 05  X  ENG  @0 Respiratory disease @5 13
C07 05  X  SPA  @0 Aparato respiratorio patología @5 13
C07 06  X  FRE  @0 Infection
C07 06  X  ENG  @0 Infection
C07 06  X  SPA  @0 Infección
C07 07  X  FRE  @0 Poumon pathologie @5 16
C07 07  X  ENG  @0 Lung disease @5 16
C07 07  X  SPA  @0 Pulmón patología @5 16
N21       @1 163
N44 01      @1 OTO
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Pascal:06-0257225

Le document en format XML

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<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.</div>
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<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="02">
<s1>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University</s1>
<s2>Hokkaido</s2>
<s3>JPN</s3>
<sZ>2 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="03">
<s1>Department of Pediatrics, Sapporo Medical University School of Medicine</s1>
<s2>Hokkaido</s2>
<s3>JPN</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA20>
<s1>417-424</s1>
</fA20>
<fA21>
<s1>2006</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>17422</s2>
<s5>354000153370750010</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2006 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>1 p.1/4</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>06-0257225</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Journal of medical virology</s0>
</fA64>
<fA66 i1="01">
<s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>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.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002A05C10</s0>
</fC02>
<fC02 i1="02" i2="X">
<s0>002B05C02J</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Virus syndrome respiratoire aigu sévère</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Severe acute respiratory syndrome virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Severe acute respiratory syndrome virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Cytokine</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Cytokine</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Citoquina</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Interleukine 6</s0>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Interleukin 6</s0>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Interleuquina 6</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Virose</s0>
<s5>14</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Viral disease</s0>
<s5>14</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Virosis</s0>
<s5>14</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>15</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>15</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Síndrome respiratorio agudo severo</s0>
<s2>NM</s2>
<s5>15</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Coronavirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Coronavirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Coronavirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Appareil respiratoire pathologie</s0>
<s5>13</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Respiratory disease</s0>
<s5>13</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Aparato respiratorio patología</s0>
<s5>13</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Infección</s0>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Poumon pathologie</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Lung disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Pulmón patología</s0>
<s5>16</s5>
</fC07>
<fN21>
<s1>163</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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