Delayed induction of proinflammatory cytokines and suppression of innate antiviral response by the novel Middle East respiratory syndrome coronavirus: implications for pathogenesis and treatment.
Identifieur interne : 001968 ( Main/Exploration ); précédent : 001967; suivant : 001969Delayed induction of proinflammatory cytokines and suppression of innate antiviral response by the novel Middle East respiratory syndrome coronavirus: implications for pathogenesis and treatment.
Auteurs : Susanna K P. Lau [République populaire de Chine] ; Candy C Y. Lau [République populaire de Chine] ; Kwok-Hung Chan [République populaire de Chine] ; Clara P Y. Li [République populaire de Chine] ; Honglin Chen [République populaire de Chine] ; Dong-Yan Jin [République populaire de Chine] ; Jasper F W. Chan [République populaire de Chine] ; Patrick C Y. Woo [République populaire de Chine] ; Kwok-Yung Yuen [République populaire de Chine]Source :
- The Journal of general virology [ 1465-2099 ] ; 2013.
Descripteurs français
- KwdFr :
- Bronches (cytologie), Bronches (virologie), Cellules épithéliales (immunologie), Cellules épithéliales (virologie), Charge virale, Coronavirus (immunologie), Coronavirus (pathogénicité), Coronavirus (physiologie), Cytokines (génétique), Cytokines (métabolisme), Fibroblastes (virologie), Humains, Immunité innée, Inflammation (immunologie), Inflammation (métabolisme), Lignée cellulaire, Moyen Orient, Régulation de l'expression des gènes (immunologie), Réplication virale, Syndrome respiratoire aigu sévère (), Syndrome respiratoire aigu sévère (immunologie).
- MESH :
- cytologie : Bronches.
- génétique : Cytokines.
- immunologie : Cellules épithéliales, Coronavirus, Inflammation, Régulation de l'expression des gènes, Syndrome respiratoire aigu sévère.
- métabolisme : Cytokines, Inflammation.
- pathogénicité : Coronavirus.
- physiologie : Coronavirus.
- virologie : Bronches, Cellules épithéliales, Fibroblastes.
- Charge virale, Humains, Immunité innée, Lignée cellulaire, Moyen Orient, Réplication virale, Syndrome respiratoire aigu sévère.
English descriptors
- KwdEn :
- Bronchi (cytology), Bronchi (virology), Cell Line, Coronavirus (immunology), Coronavirus (pathogenicity), Coronavirus (physiology), Cytokines (genetics), Cytokines (metabolism), Epithelial Cells (immunology), Epithelial Cells (virology), Fibroblasts (virology), Gene Expression Regulation (immunology), Humans, Immunity, Innate, Inflammation (immunology), Inflammation (metabolism), Middle East, Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (therapy), Viral Load, Virus Replication.
- MESH :
- chemical , genetics : Cytokines.
- geographic : Middle East.
- cytology : Bronchi.
- immunology : Coronavirus, Epithelial Cells, Gene Expression Regulation, Inflammation, Severe Acute Respiratory Syndrome.
- chemical , metabolism : Cytokines, Inflammation.
- pathogenicity : Coronavirus.
- physiology : Coronavirus.
- therapy : Severe Acute Respiratory Syndrome.
- virology : Bronchi, Epithelial Cells, Fibroblasts.
- Cell Line, Humans, Immunity, Innate, Viral Load, Virus Replication.
Abstract
The high mortality associated with the novel Middle East respiratory syndrome coronavirus (MERS-CoV) has raised questions about the possible role of a cytokine storm in its pathogenesis. Although recent studies showed that MERS-CoV infection is associated with an attenuated IFN response, no induction of inflammatory cytokines was demonstrated during the early phase of infection. To study both early and late cytokine responses associated with MERS-CoV infection, we measured the mRNA levels of eight cytokine genes [TNF-α, IL-1β, IL-6, IL-8, IFN-β, monocyte chemotactic protein-1, transforming growth factor-β and IFN-γ-induced protein (IP)-10] in cell lysates of polarized airway epithelial Calu-3 cells infected with MERS-CoV or severe acute respiratory syndrome (SARS)-CoV up to 30 h post-infection. Among the eight cytokine genes, IL-1β, IL-6 and IL-8 induced by MERS-CoV were markedly higher than those induced by SARS-CoV at 30 h, whilst TNF-α, IFN-β and IP-10 induced by SARS-CoV were markedly higher than those induced by MERS-CoV at 24 and 30 h in infected Calu-3 cells. The activation of IL-8 and attenuated IFN-β response by MERS-CoV were also confirmed by protein measurements in the culture supernatant when compared with SARS-CoV and Sendai virus. To further confirm the attenuated antiviral response, cytokine response was compared with human HCoV-229E in embryonal lung fibroblast HFL cells, which also revealed higher IFN-β and IP-10 levels induced by HCoV-229E than MERS-CoV at 24 and 30 h. Whilst our data supported recent findings that MERS-CoV elicits attenuated innate immunity, this represents the first report to demonstrate delayed proinflammatory cytokine induction by MERS-CoV. Our results provide insights into the pathogenesis and treatment of MERS-CoV infections.
DOI: 10.1099/vir.0.055533-0
PubMed: 24077366
Affiliations:
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Le document en format XML
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Lau</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, University of Hong Kong, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Lau, Candy C Y" sort="Lau, Candy C Y" uniqKey="Lau C" first="Candy C Y" last="Lau">Candy C Y. Lau</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, University of Hong Kong, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Chan, Kwok Hung" sort="Chan, Kwok Hung" uniqKey="Chan K" first="Kwok-Hung" last="Chan">Kwok-Hung Chan</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, University of Hong Kong, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Li, Clara P Y" sort="Li, Clara P Y" uniqKey="Li C" first="Clara P Y" last="Li">Clara P Y. 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China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Research Centre of Infection and Immunology, University of Hong Kong, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Jin, Dong Yan" sort="Jin, Dong Yan" uniqKey="Jin D" first="Dong-Yan" last="Jin">Dong-Yan Jin</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry, University of Hong Kong, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Chan, Jasper F W" sort="Chan, Jasper F W" uniqKey="Chan J" first="Jasper F W" last="Chan">Jasper F W. Chan</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, University of Hong Kong, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Woo, Patrick C Y" sort="Woo, Patrick C Y" uniqKey="Woo P" first="Patrick C Y" last="Woo">Patrick C Y. Woo</name><affiliation wicri:level="1"><nlm:affiliation>Carol Yu Centre for Infection, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Carol Yu Centre for Infection, University of Hong Kong, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Emerging Infectious Diseases, University of Hong Kong, Hong Kong, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Emerging Infectious Diseases, University of Hong Kong, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author></analytic><series><title level="j">The Journal of general virology</title><idno type="eISSN">1465-2099</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Bronchi (cytology)</term><term>Bronchi (virology)</term><term>Cell Line</term><term>Coronavirus (immunology)</term><term>Coronavirus (pathogenicity)</term><term>Coronavirus (physiology)</term><term>Cytokines (genetics)</term><term>Cytokines (metabolism)</term><term>Epithelial Cells (immunology)</term><term>Epithelial Cells (virology)</term><term>Fibroblasts (virology)</term><term>Gene Expression Regulation (immunology)</term><term>Humans</term><term>Immunity, Innate</term><term>Inflammation (immunology)</term><term>Inflammation (metabolism)</term><term>Middle East</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (therapy)</term><term>Viral Load</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Bronches (cytologie)</term><term>Bronches (virologie)</term><term>Cellules épithéliales (immunologie)</term><term>Cellules épithéliales (virologie)</term><term>Charge virale</term><term>Coronavirus (immunologie)</term><term>Coronavirus (pathogénicité)</term><term>Coronavirus (physiologie)</term><term>Cytokines (génétique)</term><term>Cytokines (métabolisme)</term><term>Fibroblastes (virologie)</term><term>Humains</term><term>Immunité innée</term><term>Inflammation (immunologie)</term><term>Inflammation (métabolisme)</term><term>Lignée cellulaire</term><term>Moyen Orient</term><term>Régulation de l'expression des gènes (immunologie)</term><term>Réplication virale</term><term>Syndrome respiratoire aigu sévère ()</term><term>Syndrome respiratoire aigu sévère (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" type="geographic" xml:lang="en"><term>Middle East</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Bronches</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Bronchi</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules épithéliales</term><term>Coronavirus</term><term>Inflammation</term><term>Régulation de l'expression des gènes</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Coronavirus</term><term>Epithelial Cells</term><term>Gene Expression Regulation</term><term>Inflammation</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Bronches</term><term>Cellules épithéliales</term><term>Fibroblastes</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Bronchi</term><term>Epithelial Cells</term><term>Fibroblasts</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Humans</term><term>Immunity, Innate</term><term>Viral Load</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Charge virale</term><term>Humains</term><term>Immunité innée</term><term>Lignée cellulaire</term><term>Moyen Orient</term><term>Réplication virale</term><term>Syndrome respiratoire aigu sévère</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The high mortality associated with the novel Middle East respiratory syndrome coronavirus (MERS-CoV) has raised questions about the possible role of a cytokine storm in its pathogenesis. Although recent studies showed that MERS-CoV infection is associated with an attenuated IFN response, no induction of inflammatory cytokines was demonstrated during the early phase of infection. To study both early and late cytokine responses associated with MERS-CoV infection, we measured the mRNA levels of eight cytokine genes [TNF-α, IL-1β, IL-6, IL-8, IFN-β, monocyte chemotactic protein-1, transforming growth factor-β and IFN-γ-induced protein (IP)-10] in cell lysates of polarized airway epithelial Calu-3 cells infected with MERS-CoV or severe acute respiratory syndrome (SARS)-CoV up to 30 h post-infection. Among the eight cytokine genes, IL-1β, IL-6 and IL-8 induced by MERS-CoV were markedly higher than those induced by SARS-CoV at 30 h, whilst TNF-α, IFN-β and IP-10 induced by SARS-CoV were markedly higher than those induced by MERS-CoV at 24 and 30 h in infected Calu-3 cells. The activation of IL-8 and attenuated IFN-β response by MERS-CoV were also confirmed by protein measurements in the culture supernatant when compared with SARS-CoV and Sendai virus. To further confirm the attenuated antiviral response, cytokine response was compared with human HCoV-229E in embryonal lung fibroblast HFL cells, which also revealed higher IFN-β and IP-10 levels induced by HCoV-229E than MERS-CoV at 24 and 30 h. Whilst our data supported recent findings that MERS-CoV elicits attenuated innate immunity, this represents the first report to demonstrate delayed proinflammatory cytokine induction by MERS-CoV. Our results provide insights into the pathogenesis and treatment of MERS-CoV infections. </div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Lau, Susanna K P" sort="Lau, Susanna K P" uniqKey="Lau S" first="Susanna K P" last="Lau">Susanna K P. Lau</name></noRegion><name sortKey="Chan, Jasper F W" sort="Chan, Jasper F W" uniqKey="Chan J" first="Jasper F W" last="Chan">Jasper F W. Chan</name><name sortKey="Chan, Kwok Hung" sort="Chan, Kwok Hung" uniqKey="Chan K" first="Kwok-Hung" last="Chan">Kwok-Hung Chan</name><name sortKey="Chen, Honglin" sort="Chen, Honglin" uniqKey="Chen H" first="Honglin" last="Chen">Honglin Chen</name><name sortKey="Jin, Dong Yan" sort="Jin, Dong Yan" uniqKey="Jin D" first="Dong-Yan" last="Jin">Dong-Yan Jin</name><name sortKey="Lau, Candy C Y" sort="Lau, Candy C Y" uniqKey="Lau C" first="Candy C Y" last="Lau">Candy C Y. Lau</name><name sortKey="Li, Clara P Y" sort="Li, Clara P Y" uniqKey="Li C" first="Clara P Y" last="Li">Clara P Y. Li</name><name sortKey="Woo, Patrick C Y" sort="Woo, Patrick C Y" uniqKey="Woo P" first="Patrick C Y" last="Woo">Patrick C Y. Woo</name><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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