Up-regulation of IL-6 and TNF-α induced by SARS-coronavirus spike protein in murine macrophages via NF-κB pathway
Identifieur interne : 001610 ( Pmc/Curation ); précédent : 001609; suivant : 001611Up-regulation of IL-6 and TNF-α induced by SARS-coronavirus spike protein in murine macrophages via NF-κB pathway
Auteurs : Wei Wang ; Linbai Ye ; Li Ye ; Baozong Li ; Bo Gao ; Yingchun Zeng ; Lingbao Kong ; Xiaonan Fang ; Hong Zheng ; Zhenghui Wu ; Yinglong SheSource :
- Virus Research [ 0168-1702 ] ; 2007.
Abstract
The clinical picture of severe acute respiratory syndrome (SARS) is characterized by an over-exuberant immune response with lung lymphomononuclear cells infilteration and proliferation that may account for tissue damage more than the direct effect of viral replication. To understand how cells response in the early stage of virus–host cell interaction, in this study, a purified recombinant S protein was studied for stimulating murine macrophages (RAW264.7) to produce proinflammatory cytokines (IL-6 and TNF-α) and chemokine IL-8. We found that direct induction of IL-6 and TNF-α release in the supernatant in a dose-, time-dependent manner and highly spike protein-specific, but no induction of IL-8 was detected. Further experiments showed that IL-6 and TNF-α production were dependent on NF-κB, which was activated through I-κBα degradation. These results suggest that SARS-CoV spike protein may play an important role in the pathogenesis of SARS, especially in inflammation and high fever.
Url:
DOI: 10.1016/j.virusres.2007.02.007
PubMed: 17532082
PubMed Central: 7114322
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To understand how cells response in the early stage of virus–host cell interaction, in this study, a purified recombinant S protein was studied for stimulating murine macrophages (RAW264.7) to produce proinflammatory cytokines (IL-6 and TNF-α) and chemokine IL-8. We found that direct induction of IL-6 and TNF-α release in the supernatant in a dose-, time-dependent manner and highly spike protein-specific, but no induction of IL-8 was detected. Further experiments showed that IL-6 and TNF-α production were dependent on NF-κB, which was activated through I-κBα degradation. These results suggest that SARS-CoV spike protein may play an important role in the pathogenesis of SARS, especially in inflammation and high fever.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Banerjee, S" uniqKey="Banerjee S">S. Banerjee</name></author><author><name sortKey="Narayanan, K" uniqKey="Narayanan K">K. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Virus Res</journal-id><journal-id journal-id-type="iso-abbrev">Virus Res</journal-id><journal-title-group><journal-title>Virus Research</journal-title></journal-title-group><issn pub-type="ppub">0168-1702</issn><issn pub-type="epub">1872-7492</issn><publisher><publisher-name>Published by Elsevier B.V.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">17532082</article-id><article-id pub-id-type="pmc">7114322</article-id><article-id pub-id-type="publisher-id">S0168-1702(07)00047-0</article-id><article-id pub-id-type="doi">10.1016/j.virusres.2007.02.007</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Up-regulation of IL-6 and TNF-α induced by SARS-coronavirus spike protein in murine macrophages via NF-κB pathway</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Wei</given-names></name></contrib><contrib contrib-type="author"><name><surname>Ye</surname><given-names>Linbai</given-names></name><email>linbaiye@whu.edu.cn</email><email>linbaiye@hotmail.com</email><xref rid="cor1" ref-type="corresp">⁎</xref></contrib><contrib contrib-type="author"><name><surname>Ye</surname><given-names>Li</given-names></name></contrib><contrib contrib-type="author"><name><surname>Li</surname><given-names>Baozong</given-names></name></contrib><contrib contrib-type="author"><name><surname>Gao</surname><given-names>Bo</given-names></name></contrib><contrib contrib-type="author"><name><surname>Zeng</surname><given-names>Yingchun</given-names></name></contrib><contrib contrib-type="author"><name><surname>Kong</surname><given-names>Lingbao</given-names></name></contrib><contrib contrib-type="author"><name><surname>Fang</surname><given-names>Xiaonan</given-names></name></contrib><contrib contrib-type="author"><name><surname>Zheng</surname><given-names>Hong</given-names></name></contrib><contrib contrib-type="author"><name><surname>Wu</surname><given-names>Zhenghui</given-names></name></contrib><contrib contrib-type="author"><name><surname>She</surname><given-names>Yinglong</given-names></name></contrib></contrib-group><aff>State Key Laboratory of Virology, College of Life Science, Wuhan University, Wuhan, Hubei 430072, China</aff><author-notes><corresp id="cor1"><label>⁎</label>Corresponding author. Tel.: +86 27 6875 2372; fax: +86 27 6876 4763. <email>linbaiye@whu.edu.cn</email><email>linbaiye@hotmail.com</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>25</day><month>5</month><year>2007</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><month>9</month><year>2007</year></pub-date><pub-date pub-type="epub"><day>25</day><month>5</month><year>2007</year></pub-date><volume>128</volume><issue>1</issue><fpage>1</fpage><lpage>8</lpage><history><date date-type="received"><day>3</day><month>11</month><year>2006</year></date><date date-type="rev-recd"><day>6</day><month>2</month><year>2007</year></date><date date-type="accepted"><day>8</day><month>2</month><year>2007</year></date></history><permissions><copyright-statement>Copyright © 2007 Published by Elsevier B.V.</copyright-statement><copyright-year>2007</copyright-year><copyright-holder></copyright-holder><license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p></license></permissions><abstract><p>The clinical picture of severe acute respiratory syndrome (SARS) is characterized by an over-exuberant immune response with lung lymphomononuclear cells infilteration and proliferation that may account for tissue damage more than the direct effect of viral replication. To understand how cells response in the early stage of virus–host cell interaction, in this study, a purified recombinant S protein was studied for stimulating murine macrophages (RAW264.7) to produce proinflammatory cytokines (IL-6 and TNF-α) and chemokine IL-8. We found that direct induction of IL-6 and TNF-α release in the supernatant in a dose-, time-dependent manner and highly spike protein-specific, but no induction of IL-8 was detected. Further experiments showed that IL-6 and TNF-α production were dependent on NF-κB, which was activated through I-κBα degradation. These results suggest that SARS-CoV spike protein may play an important role in the pathogenesis of SARS, especially in inflammation and high fever.</p></abstract><kwd-group><title>Keywords</title><kwd>SARS-coronavirus</kwd><kwd>Spike protein</kwd><kwd>IL-6</kwd><kwd>TNF-α</kwd><kwd>NF-κB</kwd><kwd>Macrophages</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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