Middle east respiratory syndrome corona virus spike glycoprotein suppresses macrophage responses via DPP4-mediated induction of IRAK-M and PPARγ
Identifieur interne : 000E90 ( Main/Merge ); précédent : 000E89; suivant : 000E91Middle east respiratory syndrome corona virus spike glycoprotein suppresses macrophage responses via DPP4-mediated induction of IRAK-M and PPARγ
Auteurs : Ahmed A. Al-Qahtani [Arabie saoudite] ; Konstantina Lyroni [Grèce] ; Marina Aznaourova [Grèce] ; Melpomeni Tseliou [Grèce] ; Mashael R. Al-Anazi [Arabie saoudite] ; Mohammed N. Al-Ahdal [Arabie saoudite] ; Saad Alkahtani [Arabie saoudite] ; George Sourvinos [Grèce] ; Christos Tsatsanis [Grèce]Source :
- Oncotarget [ 1949-2553 ] ; 2017.
Descripteurs français
- KwdFr :
- Activation des macrophages (), Coronavirus du syndrome respiratoire du Moyen-Orient (génétique), Coronavirus du syndrome respiratoire du Moyen-Orient (immunologie), Coronavirus du syndrome respiratoire du Moyen-Orient (métabolisme), Coronavirus du syndrome respiratoire du Moyen-Orient (pathogénicité), Dipeptidyl peptidase 4 (génétique), Dipeptidyl peptidase 4 (métabolisme), Facteur de nécrose tumorale alpha (métabolisme), Glycoprotéine de spicule des coronavirus (génétique), Glycoprotéine de spicule des coronavirus (métabolisme), Humains, Inhibiteurs de la dipeptidyl-peptidase IV (pharmacologie), Interactions hôte-pathogène, Interférence par ARN, Interleukin-1 Receptor-Associated Kinases (génétique), Interleukin-1 Receptor-Associated Kinases (métabolisme), Interleukine-10 (métabolisme), Interleukine-6 (métabolisme), Macrophages (), Macrophages (enzymologie), Macrophages (immunologie), Macrophages (virologie), Récepteur PPAR gamma (génétique), Récepteur PPAR gamma (métabolisme), Transduction du signal, Transfection.
- MESH :
- enzymologie : Macrophages.
- génétique : Coronavirus du syndrome respiratoire du Moyen-Orient, Dipeptidyl peptidase 4, Glycoprotéine de spicule des coronavirus, Interleukin-1 Receptor-Associated Kinases, Récepteur PPAR gamma.
- immunologie : Coronavirus du syndrome respiratoire du Moyen-Orient, Macrophages.
- métabolisme : Coronavirus du syndrome respiratoire du Moyen-Orient, Dipeptidyl peptidase 4, Facteur de nécrose tumorale alpha, Glycoprotéine de spicule des coronavirus, Interleukin-1 Receptor-Associated Kinases, Interleukine-10, Interleukine-6, Récepteur PPAR gamma.
- pathogénicité : Coronavirus du syndrome respiratoire du Moyen-Orient.
- pharmacologie : Inhibiteurs de la dipeptidyl-peptidase IV.
- virologie : Macrophages.
- Activation des macrophages, Humains, Interactions hôte-pathogène, Interférence par ARN, Macrophages, Transduction du signal, Transfection.
English descriptors
- KwdEn :
- Dipeptidyl Peptidase 4 (genetics), Dipeptidyl Peptidase 4 (metabolism), Dipeptidyl-Peptidase IV Inhibitors (pharmacology), Host-Pathogen Interactions, Humans, Interleukin-1 Receptor-Associated Kinases (genetics), Interleukin-1 Receptor-Associated Kinases (metabolism), Interleukin-10 (metabolism), Interleukin-6 (metabolism), Macrophage Activation (drug effects), Macrophages (drug effects), Macrophages (enzymology), Macrophages (immunology), Macrophages (virology), Middle East Respiratory Syndrome Coronavirus (genetics), Middle East Respiratory Syndrome Coronavirus (immunology), Middle East Respiratory Syndrome Coronavirus (metabolism), Middle East Respiratory Syndrome Coronavirus (pathogenicity), PPAR gamma (genetics), PPAR gamma (metabolism), RNA Interference, Signal Transduction, Spike Glycoprotein, Coronavirus (genetics), Spike Glycoprotein, Coronavirus (metabolism), THP-1 Cells, Transfection, Tumor Necrosis Factor-alpha (metabolism).
- MESH :
- chemical , genetics : Dipeptidyl Peptidase 4, Interleukin-1 Receptor-Associated Kinases, PPAR gamma, Spike Glycoprotein, Coronavirus.
- chemical , metabolism : Dipeptidyl Peptidase 4, Interleukin-1 Receptor-Associated Kinases, Interleukin-10, Interleukin-6, PPAR gamma, Spike Glycoprotein, Coronavirus, Tumor Necrosis Factor-alpha.
- chemical , pharmacology : Dipeptidyl-Peptidase IV Inhibitors.
- drug effects : Macrophage Activation, Macrophages.
- enzymology : Macrophages.
- genetics : Middle East Respiratory Syndrome Coronavirus.
- immunology : Macrophages, Middle East Respiratory Syndrome Coronavirus.
- metabolism : Middle East Respiratory Syndrome Coronavirus.
- pathogenicity : Middle East Respiratory Syndrome Coronavirus.
- virology : Macrophages.
- Host-Pathogen Interactions, Humans, RNA Interference, Signal Transduction, THP-1 Cells, Transfection.
Abstract
Middle East Respiratory Syndrome Corona Virus (MERS-CoV) is transmitted
Url:
DOI: 10.18632/oncotarget.14754
PubMed: 28118607
PubMed Central: 5354714
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PMC:5354714Le document en format XML
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<term>Host-Pathogen Interactions</term>
<term>Humans</term>
<term>Interleukin-1 Receptor-Associated Kinases (genetics)</term>
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<term>Interleukin-10 (metabolism)</term>
<term>Interleukin-6 (metabolism)</term>
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<term>Macrophages (immunology)</term>
<term>Macrophages (virology)</term>
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<term>Middle East Respiratory Syndrome Coronavirus (pathogenicity)</term>
<term>PPAR gamma (genetics)</term>
<term>PPAR gamma (metabolism)</term>
<term>RNA Interference</term>
<term>Signal Transduction</term>
<term>Spike Glycoprotein, Coronavirus (genetics)</term>
<term>Spike Glycoprotein, Coronavirus (metabolism)</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Coronavirus du syndrome respiratoire du Moyen-Orient</term>
<term>Dipeptidyl peptidase 4</term>
<term>Facteur de nécrose tumorale alpha</term>
<term>Glycoprotéine de spicule des coronavirus</term>
<term>Interleukin-1 Receptor-Associated Kinases</term>
<term>Interleukine-10</term>
<term>Interleukine-6</term>
<term>Récepteur PPAR gamma</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Coronavirus du syndrome respiratoire du Moyen-Orient</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Inhibiteurs de la dipeptidyl-peptidase IV</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>Host-Pathogen Interactions</term>
<term>Humans</term>
<term>RNA Interference</term>
<term>Signal Transduction</term>
<term>THP-1 Cells</term>
<term>Transfection</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Activation des macrophages</term>
<term>Humains</term>
<term>Interactions hôte-pathogène</term>
<term>Interférence par ARN</term>
<term>Macrophages</term>
<term>Transduction du signal</term>
<term>Transfection</term>
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<front><div type="abstract" xml:lang="en"><p>Middle East Respiratory Syndrome Corona Virus (MERS-CoV) is transmitted <italic>via</italic>
the respiratory tract and causes severe Acute Respiratory Distress Syndrome by infecting lung epithelial cells and macrophages. Macrophages can readily recognize the virus and eliminate it. MERS-CoV infects cells <italic>via</italic>
its Spike (S) glycoprotein that binds on Dipeptidyl-Peptidase 4 (DPP4) receptor present on macrophages. Whether this Spike/DPP4 association affects macrophage responses remains unknown. Herein we demonstrated that infection of macrophages with lentiviral particles pseudotyped with MERS-CoV S glycoprotein results in suppression of macrophage responses since it reduced the capacity of macrophages to produce TNFa and IL-6 in naive and LPS-activated THP-1 macrophages and augmented LPS-induced production of the immunosuppressive cytokine IL-10. MERS-CoV S glycoprotein induced the expression of the negative regulator of TLR signaling IRAK-M as well as of the transcriptional repressor PPARγ. Inhibition of DPP4 by its inhibitor sitagliptin or siRNA abrogated the effects of MERS-CoV S glycoprotein on IRAK-M, PPARγ and IL-10, confirming that its immunosuppressive effects were mediated by DPP4 receptor. The effect was observed both in THP-1 macrophages and human primary peripheral blood monocytes. These findings support a DPP4-mediated suppressive action of MERS-CoV in macrophages and suggest a potential target for effective elimination of its pathogenicity.</p>
</div>
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