Middle east respiratory syndrome corona virus spike glycoprotein suppresses macrophage responses via DPP4-mediated induction of IRAK-M and PPARγ.
Identifieur interne : 000C69 ( PubMed/Curation ); 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 [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 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
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<term>Dipeptidyl Peptidase 4 (metabolism)</term>
<term>Dipeptidyl-Peptidase IV Inhibitors (pharmacology)</term>
<term>Host-Pathogen Interactions</term>
<term>Humans</term>
<term>Interleukin-1 Receptor-Associated Kinases (genetics)</term>
<term>Interleukin-1 Receptor-Associated Kinases (metabolism)</term>
<term>Interleukin-10 (metabolism)</term>
<term>Interleukin-6 (metabolism)</term>
<term>Macrophage Activation (drug effects)</term>
<term>Macrophages (drug effects)</term>
<term>Macrophages (enzymology)</term>
<term>Macrophages (immunology)</term>
<term>Macrophages (virology)</term>
<term>Middle East Respiratory Syndrome Coronavirus (genetics)</term>
<term>Middle East Respiratory Syndrome Coronavirus (immunology)</term>
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<term>PPAR gamma (metabolism)</term>
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<term>Macrophages (immunologie)</term>
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<term>Spike Glycoprotein, Coronavirus</term>
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<term>Dipeptidyl peptidase 4</term>
<term>Facteur de nécrose tumorale alpha</term>
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<term>Interleukin-1 Receptor-Associated Kinases</term>
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<term>Humains</term>
<term>Interactions hôte-pathogène</term>
<term>Interférence par ARN</term>
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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>
</front>
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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>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Al-Qahtani</LastName>
<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>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, School of Medicine, Alfaisal University, Riyadh, Saudi Arabia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lyroni</LastName>
<ForeName>Konstantina</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Laboratory of Clinical Chemistry, Medical School, University of Crete, Heraklion, Greece.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Aznaourova</LastName>
<ForeName>Marina</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Laboratory of Clinical Chemistry, Medical School, University of Crete, Heraklion, Greece.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tseliou</LastName>
<ForeName>Melpomeni</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Laboratory of Virology, Medical School, University of Crete, Heraklion, Greece.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Al-Anazi</LastName>
<ForeName>Mashael R</ForeName>
<Initials>MR</Initials>
<AffiliationInfo><Affiliation>Department of Infection and Immunity, Research Center, King Faisal Specialist Hospital and Research Center, Saudi Arabia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Al-Ahdal</LastName>
<ForeName>Mohammed N</ForeName>
<Initials>MN</Initials>
<AffiliationInfo><Affiliation>Department of Infection and Immunity, Research Center, King Faisal Specialist Hospital and Research Center, Saudi Arabia.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, School of Medicine, Alfaisal University, Riyadh, Saudi Arabia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Alkahtani</LastName>
<ForeName>Saad</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Zoology Department, College of Science, King Saud University, Riyadh, Saudi Arabia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sourvinos</LastName>
<ForeName>George</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Laboratory of Virology, Medical School, University of Crete, Heraklion, Greece.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tsatsanis</LastName>
<ForeName>Christos</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Laboratory of Clinical Chemistry, Medical School, University of Crete, Heraklion, Greece.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Oncotarget</MedlineTA>
<NlmUniqueID>101532965</NlmUniqueID>
<ISSNLinking>1949-2553</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054873">Dipeptidyl-Peptidase IV Inhibitors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C508609">IL10 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C508600">IL6 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D047495">PPAR gamma</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D064370">Spike Glycoprotein, Coronavirus</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>130068-27-8</RegistryNumber>
<NameOfSubstance UI="D016753">Interleukin-10</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="C507771">IRAK3 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D053592">Interleukin-1 Receptor-Associated Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.14.5</RegistryNumber>
<NameOfSubstance UI="C042807">DPP4 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.14.5</RegistryNumber>
<NameOfSubstance UI="D018819">Dipeptidyl Peptidase 4</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D018819" MajorTopicYN="N">Dipeptidyl Peptidase 4</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054873" MajorTopicYN="N">Dipeptidyl-Peptidase IV Inhibitors</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054884" MajorTopicYN="N">Host-Pathogen Interactions</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053592" MajorTopicYN="N">Interleukin-1 Receptor-Associated Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016753" MajorTopicYN="N">Interleukin-10</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015850" MajorTopicYN="N">Interleukin-6</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008262" MajorTopicYN="Y">Macrophage Activation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D065207" MajorTopicYN="N">Middle East Respiratory Syndrome Coronavirus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D047495" MajorTopicYN="N">PPAR gamma</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D034622" MajorTopicYN="N">RNA Interference</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D064370" MajorTopicYN="N">Spike Glycoprotein, Coronavirus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000074084" MajorTopicYN="N">THP-1 Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014162" MajorTopicYN="N">Transfection</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014409" MajorTopicYN="N">Tumor Necrosis Factor-alpha</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">DPP4</Keyword>
<Keyword MajorTopicYN="N">IRAK-M</Keyword>
<Keyword MajorTopicYN="N">Immune response</Keyword>
<Keyword MajorTopicYN="N">Immunity</Keyword>
<Keyword MajorTopicYN="N">Immunology and Microbiology Section</Keyword>
<Keyword MajorTopicYN="N">MERS CoV</Keyword>
<Keyword MajorTopicYN="N">cytokines</Keyword>
<Keyword MajorTopicYN="N">macrophages</Keyword>
</KeywordList>
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<Month>01</Month>
<Day>10</Day>
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