Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections
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 incl...
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| Veröffentlicht in: | Journal of medical virology 2006-04, Vol.78 (4), p.417-424 |
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| creator | Okabayashi, Tamaki Kariwa, Hiroaki Yokota, Shin-ichi Iki, Shigeo Indoh, Tomokazu Yokosawa, Noriko Takashima, Ikuo Tsutsumi, Hiroyuki Fujii, Nobuhiro |
| description | 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. |
| doi_str_mv | 10.1002/jmv.20556 |
| format | Article |
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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.</description><identifier>ISSN: 0146-6615</identifier><identifier>EISSN: 1096-9071</identifier><identifier>DOI: 10.1002/jmv.20556</identifier><identifier>PMID: 16482545</identifier><identifier>CODEN: JMVIDB</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Biological and medical sciences ; Caco-2 Cells ; Cell Line, Tumor ; cytokine ; Cytokines - genetics ; Cytokines - metabolism ; Fundamental and applied biological sciences. Psychology ; Gene Expression Profiling ; Human viral diseases ; Humans ; IFN ; IL-6 ; Infectious diseases ; Influenza A virus ; Interferons - genetics ; Interferons - metabolism ; Medical sciences ; Microbiology ; Miscellaneous ; Parainfluenza virus ; Respiratory syncytial virus ; Respiratory Tract Infections - immunology ; Respiratory Tract Infections - virology ; SARS coronavirus ; SARS Virus - pathogenicity ; SARS-CoV ; Severe Acute Respiratory Syndrome - immunology ; Severe Acute Respiratory Syndrome - virology ; SOCS3 ; TLR ; Viral diseases ; Virology ; Virus Diseases - immunology ; Virus Diseases - virology ; Virus Replication</subject><ispartof>Journal of medical virology, 2006-04, Vol.78 (4), p.417-424</ispartof><rights>Copyright © 2006 Wiley‐Liss, Inc.</rights><rights>2006 INIST-CNRS</rights><rights>Copyright 2006 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5786-76bc6a7756a37e49fdd559c7d71b6cf67aa285548e6393eaf4eb3e3ec2701f0c3</citedby><cites>FETCH-LOGICAL-c5786-76bc6a7756a37e49fdd559c7d71b6cf67aa285548e6393eaf4eb3e3ec2701f0c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjmv.20556$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjmv.20556$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,777,781,882,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17585778$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16482545$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Okabayashi, Tamaki</creatorcontrib><creatorcontrib>Kariwa, Hiroaki</creatorcontrib><creatorcontrib>Yokota, Shin-ichi</creatorcontrib><creatorcontrib>Iki, Shigeo</creatorcontrib><creatorcontrib>Indoh, Tomokazu</creatorcontrib><creatorcontrib>Yokosawa, Noriko</creatorcontrib><creatorcontrib>Takashima, Ikuo</creatorcontrib><creatorcontrib>Tsutsumi, Hiroyuki</creatorcontrib><creatorcontrib>Fujii, Nobuhiro</creatorcontrib><title>Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections</title><title>Journal of medical virology</title><addtitle>J. Med. Virol</addtitle><description>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.</description><subject>Biological and medical sciences</subject><subject>Caco-2 Cells</subject><subject>Cell Line, Tumor</subject><subject>cytokine</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Profiling</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>IFN</subject><subject>IL-6</subject><subject>Infectious diseases</subject><subject>Influenza A virus</subject><subject>Interferons - genetics</subject><subject>Interferons - metabolism</subject><subject>Medical sciences</subject><subject>Microbiology</subject><subject>Miscellaneous</subject><subject>Parainfluenza virus</subject><subject>Respiratory syncytial virus</subject><subject>Respiratory Tract Infections - immunology</subject><subject>Respiratory Tract Infections - virology</subject><subject>SARS coronavirus</subject><subject>SARS Virus - pathogenicity</subject><subject>SARS-CoV</subject><subject>Severe Acute Respiratory Syndrome - immunology</subject><subject>Severe Acute Respiratory Syndrome - virology</subject><subject>SOCS3</subject><subject>TLR</subject><subject>Viral diseases</subject><subject>Virology</subject><subject>Virus Diseases - immunology</subject><subject>Virus Diseases - virology</subject><subject>Virus Replication</subject><issn>0146-6615</issn><issn>1096-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9v1DAQxS0EotvCgS-AcgGph7R2HHucC1K70BZUQLD8uxmvM2ndJvFiJwv77XG7SwtIiJMlz--9N6NHyCNG9xilxf5Ft9wrqBDyDpkwWsm8osDukgllpcylZGKLbMd4QSlVVVHcJ1tMlqoQpZiQr9PV4C9dj1nAs7E1g_N95vpsdvB-llkffG-WLowx_TVor6fWdwsTsM4Gn_nhHEOSxoULZvBhlf1FxwfkXmPaiA837w75ePTiw_QkP317_HJ6cJpbAUrmIOdWGgAhDQcsq6auhags1MDm0jYSjCmUEKVCySuOpilxzpGjLYCyhlq-Q56tfRfjvMPaYj8E0-pFcJ0JK-2N039Oeneuz_xSA5MSQCaDpxuD4L-NGAfduWixbU2Pfow6QRXw8v9gaoIzpVQCd9egDT7GgM3NNozqq-J0Kk5fF5fYx7-vf0tumkrAkw1gojVtE0xvXbzlQCgBcBW6v-a-uxZX_07Ur15_-hWdrxUuDvjjRmHCZbqZg9Cf3xzro3eHbPbl5LmW_CeAK8HE</recordid><startdate>200604</startdate><enddate>200604</enddate><creator>Okabayashi, Tamaki</creator><creator>Kariwa, Hiroaki</creator><creator>Yokota, Shin-ichi</creator><creator>Iki, Shigeo</creator><creator>Indoh, Tomokazu</creator><creator>Yokosawa, Noriko</creator><creator>Takashima, Ikuo</creator><creator>Tsutsumi, Hiroyuki</creator><creator>Fujii, Nobuhiro</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200604</creationdate><title>Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections</title><author>Okabayashi, Tamaki ; Kariwa, Hiroaki ; Yokota, Shin-ichi ; Iki, Shigeo ; Indoh, Tomokazu ; Yokosawa, Noriko ; Takashima, Ikuo ; Tsutsumi, Hiroyuki ; Fujii, Nobuhiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5786-76bc6a7756a37e49fdd559c7d71b6cf67aa285548e6393eaf4eb3e3ec2701f0c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Biological and medical sciences</topic><topic>Caco-2 Cells</topic><topic>Cell Line, Tumor</topic><topic>cytokine</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Profiling</topic><topic>Human viral diseases</topic><topic>Humans</topic><topic>IFN</topic><topic>IL-6</topic><topic>Infectious diseases</topic><topic>Influenza A virus</topic><topic>Interferons - genetics</topic><topic>Interferons - metabolism</topic><topic>Medical sciences</topic><topic>Microbiology</topic><topic>Miscellaneous</topic><topic>Parainfluenza virus</topic><topic>Respiratory syncytial virus</topic><topic>Respiratory Tract Infections - immunology</topic><topic>Respiratory Tract Infections - virology</topic><topic>SARS coronavirus</topic><topic>SARS Virus - pathogenicity</topic><topic>SARS-CoV</topic><topic>Severe Acute Respiratory Syndrome - immunology</topic><topic>Severe Acute Respiratory Syndrome - virology</topic><topic>SOCS3</topic><topic>TLR</topic><topic>Viral diseases</topic><topic>Virology</topic><topic>Virus Diseases - immunology</topic><topic>Virus Diseases - virology</topic><topic>Virus Replication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Okabayashi, Tamaki</creatorcontrib><creatorcontrib>Kariwa, Hiroaki</creatorcontrib><creatorcontrib>Yokota, Shin-ichi</creatorcontrib><creatorcontrib>Iki, Shigeo</creatorcontrib><creatorcontrib>Indoh, Tomokazu</creatorcontrib><creatorcontrib>Yokosawa, Noriko</creatorcontrib><creatorcontrib>Takashima, Ikuo</creatorcontrib><creatorcontrib>Tsutsumi, Hiroyuki</creatorcontrib><creatorcontrib>Fujii, Nobuhiro</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of medical virology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Okabayashi, Tamaki</au><au>Kariwa, Hiroaki</au><au>Yokota, Shin-ichi</au><au>Iki, Shigeo</au><au>Indoh, Tomokazu</au><au>Yokosawa, Noriko</au><au>Takashima, Ikuo</au><au>Tsutsumi, Hiroyuki</au><au>Fujii, Nobuhiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections</atitle><jtitle>Journal of medical virology</jtitle><addtitle>J. Med. Virol</addtitle><date>2006-04</date><risdate>2006</risdate><volume>78</volume><issue>4</issue><spage>417</spage><epage>424</epage><pages>417-424</pages><issn>0146-6615</issn><eissn>1096-9071</eissn><coden>JMVIDB</coden><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.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>16482545</pmid><doi>10.1002/jmv.20556</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Biological and medical sciences Caco-2 Cells Cell Line, Tumor cytokine Cytokines - genetics Cytokines - metabolism Fundamental and applied biological sciences. Psychology Gene Expression Profiling Human viral diseases Humans IFN IL-6 Infectious diseases Influenza A virus Interferons - genetics Interferons - metabolism Medical sciences Microbiology Miscellaneous Parainfluenza virus Respiratory syncytial virus Respiratory Tract Infections - immunology Respiratory Tract Infections - virology SARS coronavirus SARS Virus - pathogenicity SARS-CoV Severe Acute Respiratory Syndrome - immunology Severe Acute Respiratory Syndrome - virology SOCS3 TLR Viral diseases Virology Virus Diseases - immunology Virus Diseases - virology Virus Replication |
| title | Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections |
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