Middle east respiratory syndrome corona virus spike glycoprotein suppresses macrophage responses via DPP4-mediated induction of IRAK-M and PPARγ.
Identifieur interne : 000C69 ( PubMed/Corpus ); précédent : 000C68; suivant : 000C70Middle east respiratory syndrome corona virus spike glycoprotein suppresses macrophage responses via DPP4-mediated induction of IRAK-M and PPARγ.
Auteurs : Ahmed A. Al-Qahtani ; Konstantina Lyroni ; Marina Aznaourova ; Melpomeni Tseliou ; Mashael R. Al-Anazi ; Mohammed N. Al-Ahdal ; Saad Alkahtani ; George Sourvinos ; Christos TsatsanisSource :
- Oncotarget [ 1949-2553 ] ; 2017.
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 via 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 via 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 TNFα 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.
DOI: 10.18632/oncotarget.14754
PubMed: 28118607
Links to Exploration step
pubmed:28118607Le document en format XML
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<front><div type="abstract" xml:lang="en">Middle East Respiratory Syndrome Corona Virus (MERS-CoV) is transmitted via 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 via 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 TNFα 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.</div>
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<Abstract><AbstractText>Middle East Respiratory Syndrome Corona Virus (MERS-CoV) is transmitted via 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 via 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 TNFα 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.</AbstractText>
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<ForeName>Ahmed A</ForeName>
<Initials>AA</Initials>
<AffiliationInfo><Affiliation>Department of Infection and Immunity, Research Center, King Faisal Specialist Hospital and Research Center, Saudi Arabia.</Affiliation>
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<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, School of Medicine, Alfaisal University, Riyadh, Saudi Arabia.</Affiliation>
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