Up-regulation of IL-6 and TNF-α induced by SARS-coronavirus spike protein in murine macrophages via NF-κB pathway
Identifieur interne : 003558 ( Main/Exploration ); précédent : 003557; suivant : 003559Up-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.
Descripteurs français
- KwdFr :
- Activation des macrophages, Animaux, Facteur de nécrose tumorale alpha (génétique), Facteur de nécrose tumorale alpha (métabolisme), Facteur de transcription NF-kappa B (génétique), Facteur de transcription NF-kappa B (métabolisme), Glycoprotéine de spicule des coronavirus, Glycoprotéines membranaires (génétique), Glycoprotéines membranaires (immunologie), Glycoprotéines membranaires (métabolisme), Interleukine-6 (génétique), Interleukine-6 (métabolisme), Lignée cellulaire, Macrophages (immunologie), Macrophages (virologie), Protéines de l'enveloppe virale (génétique), Protéines de l'enveloppe virale (immunologie), Protéines de l'enveloppe virale (métabolisme), Régulation de l'expression des gènes, Régulation positive, Souris, Virus du SRAS (génétique), Virus du SRAS (immunologie).
- MESH :
- génétique : Facteur de nécrose tumorale alpha, Facteur de transcription NF-kappa B, Glycoprotéines membranaires, Interleukine-6, Protéines de l'enveloppe virale, Virus du SRAS.
- immunologie : Glycoprotéines membranaires, Macrophages, Protéines de l'enveloppe virale, Virus du SRAS.
- métabolisme : Facteur de nécrose tumorale alpha, Facteur de transcription NF-kappa B, Glycoprotéines membranaires, Interleukine-6, Protéines de l'enveloppe virale.
- virologie : Macrophages.
- Activation des macrophages, Animaux, Glycoprotéine de spicule des coronavirus, Lignée cellulaire, Régulation de l'expression des gènes, Régulation positive, Souris.
English descriptors
- KwdEn :
- Animals, Cell Line, Gene Expression Regulation, Interleukin-6 (genetics), Interleukin-6 (metabolism), Macrophage Activation, Macrophages (immunology), Macrophages (virology), Membrane Glycoproteins (genetics), Membrane Glycoproteins (immunology), Membrane Glycoproteins (metabolism), Mice, NF-kappa B (genetics), NF-kappa B (metabolism), SARS Virus (genetics), SARS Virus (immunology), Spike Glycoprotein, Coronavirus, Tumor Necrosis Factor-alpha (genetics), Tumor Necrosis Factor-alpha (metabolism), Up-Regulation, Viral Envelope Proteins (genetics), Viral Envelope Proteins (immunology), Viral Envelope Proteins (metabolism).
- MESH :
- chemical , genetics : Interleukin-6, Membrane Glycoproteins, NF-kappa B, Tumor Necrosis Factor-alpha, Viral Envelope Proteins.
- chemical , immunology : Membrane Glycoproteins, Viral Envelope Proteins.
- chemical , metabolism : Interleukin-6, Membrane Glycoproteins, NF-kappa B, Tumor Necrosis Factor-alpha, Viral Envelope Proteins.
- genetics : SARS Virus.
- immunology : Macrophages, SARS Virus.
- virology : Macrophages.
- Animals, Cell Line, Gene Expression Regulation, Macrophage Activation, Mice, Spike Glycoprotein, Coronavirus, Up-Regulation.
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
Affiliations:
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Le document en format XML
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Gao</name></author><author><name sortKey="Zeng, Yingchun" sort="Zeng, Yingchun" uniqKey="Zeng Y" first="Yingchun" last="Zeng">Yingchun Zeng</name></author><author><name sortKey="Kong, Lingbao" sort="Kong, Lingbao" uniqKey="Kong L" first="Lingbao" last="Kong">Lingbao Kong</name></author><author><name sortKey="Fang, Xiaonan" sort="Fang, Xiaonan" uniqKey="Fang X" first="Xiaonan" last="Fang">Xiaonan Fang</name></author><author><name sortKey="Zheng, Hong" sort="Zheng, Hong" uniqKey="Zheng H" first="Hong" last="Zheng">Hong Zheng</name></author><author><name sortKey="Wu, Zhenghui" sort="Wu, Zhenghui" uniqKey="Wu Z" first="Zhenghui" last="Wu">Zhenghui Wu</name></author><author><name sortKey="She, Yinglong" sort="She, Yinglong" uniqKey="She Y" first="Yinglong" last="She">Yinglong She</name></author></analytic><series><title level="j">Virus Research</title><idno type="ISSN">0168-1702</idno><idno type="eISSN">1872-7492</idno><imprint><date 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Proteins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation des macrophages</term><term>Animaux</term><term>Facteur de nécrose tumorale alpha (génétique)</term><term>Facteur de nécrose tumorale alpha (métabolisme)</term><term>Facteur de transcription NF-kappa B (génétique)</term><term>Facteur de transcription NF-kappa B (métabolisme)</term><term>Glycoprotéine de spicule des coronavirus</term><term>Glycoprotéines membranaires (génétique)</term><term>Glycoprotéines membranaires (immunologie)</term><term>Glycoprotéines membranaires (métabolisme)</term><term>Interleukine-6 (génétique)</term><term>Interleukine-6 (métabolisme)</term><term>Lignée cellulaire</term><term>Macrophages (immunologie)</term><term>Macrophages (virologie)</term><term>Protéines de l'enveloppe virale (génétique)</term><term>Protéines de l'enveloppe virale (immunologie)</term><term>Protéines de l'enveloppe virale (métabolisme)</term><term>Régulation de l'expression des gènes</term><term>Régulation positive</term><term>Souris</term><term>Virus du SRAS (génétique)</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interleukin-6</term><term>Membrane Glycoproteins</term><term>NF-kappa B</term><term>Tumor Necrosis Factor-alpha</term><term>Viral Envelope Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Membrane Glycoproteins</term><term>Viral Envelope Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Interleukin-6</term><term>Membrane Glycoproteins</term><term>NF-kappa B</term><term>Tumor Necrosis Factor-alpha</term><term>Viral Envelope Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur de nécrose tumorale alpha</term><term>Facteur de transcription NF-kappa B</term><term>Glycoprotéines membranaires</term><term>Interleukine-6</term><term>Protéines de l'enveloppe virale</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Glycoprotéines membranaires</term><term>Macrophages</term><term>Protéines de l'enveloppe virale</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Macrophages</term><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de nécrose tumorale alpha</term><term>Facteur de transcription NF-kappa B</term><term>Glycoprotéines membranaires</term><term>Interleukine-6</term><term>Protéines de l'enveloppe virale</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Macrophages</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Gene Expression Regulation</term><term>Macrophage Activation</term><term>Mice</term><term>Spike Glycoprotein, Coronavirus</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Activation des macrophages</term><term>Animaux</term><term>Glycoprotéine de spicule des coronavirus</term><term>Lignée cellulaire</term><term>Régulation de l'expression des gènes</term><term>Régulation positive</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><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></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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Elias</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list></list><tree><noCountry><name sortKey="Fang, Xiaonan" sort="Fang, Xiaonan" uniqKey="Fang X" first="Xiaonan" last="Fang">Xiaonan Fang</name><name sortKey="Gao, Bo" sort="Gao, Bo" uniqKey="Gao B" first="Bo" last="Gao">Bo Gao</name><name sortKey="Kong, Lingbao" sort="Kong, Lingbao" uniqKey="Kong L" first="Lingbao" last="Kong">Lingbao Kong</name><name sortKey="Li, Baozong" sort="Li, Baozong" uniqKey="Li B" first="Baozong" last="Li">Baozong Li</name><name sortKey="She, Yinglong" sort="She, Yinglong" uniqKey="She Y" first="Yinglong" last="She">Yinglong She</name><name sortKey="Wang, Wei" sort="Wang, Wei" uniqKey="Wang W" first="Wei" last="Wang">Wei Wang</name><name sortKey="Wu, Zhenghui" sort="Wu, Zhenghui" uniqKey="Wu Z" first="Zhenghui" last="Wu">Zhenghui Wu</name><name sortKey="Ye, Li" sort="Ye, Li" uniqKey="Ye L" first="Li" last="Ye">Li Ye</name><name sortKey="Ye, Linbai" sort="Ye, Linbai" uniqKey="Ye L" first="Linbai" last="Ye">Linbai Ye</name><name sortKey="Zeng, Yingchun" sort="Zeng, Yingchun" uniqKey="Zeng Y" first="Yingchun" last="Zeng">Yingchun Zeng</name><name sortKey="Zheng, Hong" sort="Zheng, Hong" uniqKey="Zheng H" first="Hong" last="Zheng">Hong Zheng</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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