Bitter Taste Receptors (TAS2Rs) in Human Lung Macrophages: Receptor Expression and Inhibitory Effects of TAS2R Agonists
Identifieur interne : 000057 ( France/Analysis ); précédent : 000056; suivant : 000058Bitter Taste Receptors (TAS2Rs) in Human Lung Macrophages: Receptor Expression and Inhibitory Effects of TAS2R Agonists
Auteurs : Stanislas Grassin-Delyle [France] ; Hélène Salvator [France] ; Nikola Mantov [France] ; Charlotte Abrial [France] ; Marion Brollo [France] ; Christophe Faisy [France] ; Emmanuel Naline [France] ; Louis-Jean Couderc [France] ; Philippe Devillier [France]Source :
- Frontiers in Physiology [ 1664-042X ] ; 2019.
Abstract
Bitter-taste receptors (TAS2Rs) are involved in airway relaxation but are also expressed in human blood leukocytes. We studied TAS2R expression and the effects of TAS2R agonists on the lipopolysaccharide (LPS)-induced cytokine release in human lung macrophages (LMs).
Lung macrophages were isolated from patients undergoing surgery for carcinoma. We used RT-qPCR to measure transcripts of 16 TAS2Rs (TAS2Rs 3/4/5/7/8/9/10/14/19/20/31/38/39/43/45 and 46) in unstimulated and LPS-stimulated (10 ng.mL–1) LMs. The macrophages were also incubated with TAS2R agonists for 24 h. Supernatant levels of the cytokines TNF-α, CCL3, CXCL8 and IL-10 were measured using ELISAs.
The transcripts of all 16 TAS2Rs were detected in macrophages. The addition of LPS led to an increase in the expression of most TAS2Rs, which was significant for TAS2R7 and 38. Although the promiscuous TAS2R agonists, quinine and denatonium, inhibited the LPS-induced release of TNF-α, CCL3 and CXCL8, diphenidol was inactive. Partially selective agonists (dapsone, colchicine, strychnine, and chloroquine) and selective agonists [erythromycin (TAS2R10), phenanthroline (TAS2R5), ofloxacin (TAS2R9), and carisoprodol (TAS2R14)] also suppressed the LPS-induced cytokine release. In contrast, two other agonists [sodium cromoglycate (TAS2R20) and saccharin (TAS2R31 and 43)] were inactive. TAS2R agonists suppressed IL-10 production – suggesting that this anti-inflammatory cytokine is not involved in the inhibition of cytokine production.
Human LMs expressed TAS2Rs. Experiments with TAS2R agonists’ suggested the involvement of TAS2Rs 3, 4, 5, 9, 10, 14, 30, 39 and 40 in the inhibition of cytokine production. TAS2Rs may constitute new drug targets in inflammatory obstructive lung disease.
Url:
DOI: 10.3389/fphys.2019.01267
PubMed: 31632299
PubMed Central: 6783802
Affiliations:
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Hospital</institution>,<addr-line>Suresnes</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>INSERM UMR 1173, UFR Simone Veil - Santé, University Versailles Saint-Quentin, University of Paris-Saclay</institution>,<addr-line>Montigny-le-Bretonneux</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Salvator, Helene" sort="Salvator, Helene" uniqKey="Salvator H" first="Hélène" last="Salvator">Hélène Salvator</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Airway Diseases, Foch Hospital</institution>,<addr-line>Suresnes</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Laboratory of Research in Respiratory Pharmacology–UPRES EA 220, Foch Hospital, University Versailles Saint-Quentin, University of Paris-Saclay</institution>,<addr-line>Suresnes</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Mantov, Nikola" sort="Mantov, Nikola" uniqKey="Mantov N" first="Nikola" last="Mantov">Nikola Mantov</name><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Laboratory of Research in Respiratory Pharmacology–UPRES EA 220, Foch Hospital, University Versailles Saint-Quentin, University of Paris-Saclay</institution>,<addr-line>Suresnes</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Abrial, Charlotte" sort="Abrial, Charlotte" uniqKey="Abrial C" first="Charlotte" last="Abrial">Charlotte Abrial</name><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Laboratory of Research in Respiratory Pharmacology–UPRES EA 220, Foch Hospital, University Versailles Saint-Quentin, University of Paris-Saclay</institution>,<addr-line>Suresnes</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Brollo, Marion" sort="Brollo, Marion" uniqKey="Brollo M" first="Marion" last="Brollo">Marion Brollo</name><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Laboratory of Research in Respiratory Pharmacology–UPRES EA 220, Foch Hospital, University Versailles Saint-Quentin, University of Paris-Saclay</institution>,<addr-line>Suresnes</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Faisy, Christophe" sort="Faisy, Christophe" uniqKey="Faisy C" first="Christophe" last="Faisy">Christophe Faisy</name><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Laboratory of Research in Respiratory Pharmacology–UPRES EA 220, Foch Hospital, University Versailles Saint-Quentin, University of Paris-Saclay</institution>,<addr-line>Suresnes</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Naline, Emmanuel" sort="Naline, Emmanuel" uniqKey="Naline E" first="Emmanuel" last="Naline">Emmanuel Naline</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Airway Diseases, Foch Hospital</institution>,<addr-line>Suresnes</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Laboratory of Research in Respiratory Pharmacology–UPRES EA 220, Foch Hospital, University Versailles Saint-Quentin, University of Paris-Saclay</institution>,<addr-line>Suresnes</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Couderc, Louis Jean" sort="Couderc, Louis Jean" uniqKey="Couderc L" first="Louis-Jean" last="Couderc">Louis-Jean Couderc</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Airway Diseases, Foch Hospital</institution>,<addr-line>Suresnes</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Laboratory of Research in Respiratory Pharmacology–UPRES EA 220, Foch Hospital, University Versailles Saint-Quentin, University of Paris-Saclay</institution>,<addr-line>Suresnes</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Devillier, Philippe" sort="Devillier, Philippe" uniqKey="Devillier P" first="Philippe" last="Devillier">Philippe Devillier</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Airway Diseases, Foch Hospital</institution>,<addr-line>Suresnes</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Laboratory of Research in Respiratory Pharmacology–UPRES EA 220, Foch Hospital, University Versailles Saint-Quentin, University of Paris-Saclay</institution>,<addr-line>Suresnes</addr-line>,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></analytic><series><title level="j">Frontiers in Physiology</title><idno type="eISSN">1664-042X</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p>Bitter-taste receptors (TAS2Rs) are involved in airway relaxation but are also expressed in human blood leukocytes. We studied TAS2R expression and the effects of TAS2R agonists on the lipopolysaccharide (LPS)-induced cytokine release in human lung macrophages (LMs).</p></sec><sec><title>Methods</title><p>Lung macrophages were isolated from patients undergoing surgery for carcinoma. We used RT-qPCR to measure transcripts of 16 TAS2Rs (TAS2Rs 3/4/5/7/8/9/10/14/19/20/31/38/39/43/45 and 46) in unstimulated and LPS-stimulated (10 ng.mL<sup>–1</sup>) LMs. The macrophages were also incubated with TAS2R agonists for 24 h. Supernatant levels of the cytokines TNF-α, CCL3, CXCL8 and IL-10 were measured using ELISAs.</p></sec><sec><title>Results</title><p>The transcripts of all 16 TAS2Rs were detected in macrophages. The addition of LPS led to an increase in the expression of most TAS2Rs, which was significant for TAS2R7 and 38. Although the promiscuous TAS2R agonists, quinine and denatonium, inhibited the LPS-induced release of TNF-α, CCL3 and CXCL8, diphenidol was inactive. Partially selective agonists (dapsone, colchicine, strychnine, and chloroquine) and selective agonists [erythromycin (TAS2R10), phenanthroline (TAS2R5), ofloxacin (TAS2R9), and carisoprodol (TAS2R14)] also suppressed the LPS-induced cytokine release. In contrast, two other agonists [sodium cromoglycate (TAS2R20) and saccharin (TAS2R31 and 43)] were inactive. TAS2R agonists suppressed IL-10 production – suggesting that this anti-inflammatory cytokine is not involved in the inhibition of cytokine production.</p></sec><sec><title>Conclusion</title><p>Human LMs expressed TAS2Rs. Experiments with TAS2R agonists’ suggested the involvement of TAS2Rs 3, 4, 5, 9, 10, 14, 30, 39 and 40 in the inhibition of cytokine production. TAS2Rs may constitute new drug targets in inflammatory obstructive lung disease.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Abrial, C" uniqKey="Abrial C">C. Abrial</name></author><author><name sortKey="Grassin Delyle, S" uniqKey="Grassin Delyle S">S. Grassin-Delyle</name></author><author><name sortKey="Salvator, H" uniqKey="Salvator H">H. Salvator</name></author><author><name sortKey="Brollo, M" uniqKey="Brollo M">M. Brollo</name></author><author><name sortKey="Naline, E" uniqKey="Naline E">E. Naline</name></author><author><name sortKey="Devillier, P" uniqKey="Devillier P">P. Devillier</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Alexander, S P H" uniqKey="Alexander S">S. P. H. Alexander</name></author><author><name sortKey="Mathie, A" uniqKey="Mathie A">A. Mathie</name></author><author><name sortKey="Peters, J A" uniqKey="Peters J">J. A. Peters</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Allen, J N" uniqKey="Allen J">J. N. Allen</name></author><author><name sortKey="Herzyk, D J" uniqKey="Herzyk D">D. J. 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Munic</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, M" uniqKey="Yang M">M. Yang</name></author><author><name sortKey="Kumar, R K" uniqKey="Kumar R">R. K. Kumar</name></author><author><name sortKey="Hansbro, P M" uniqKey="Hansbro P">P. M. Hansbro</name></author><author><name sortKey="Foster, P S" uniqKey="Foster P">P. S. Foster</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yasutomi, M" uniqKey="Yasutomi M">M. Yasutomi</name></author><author><name sortKey="Ohshima, Y" uniqKey="Ohshima Y">Y. Ohshima</name></author><author><name sortKey="Omata, N" uniqKey="Omata N">N. Omata</name></author><author><name sortKey="Yamada, A" uniqKey="Yamada A">A. Yamada</name></author><author><name sortKey="Iwasaki, H" uniqKey="Iwasaki H">H. Iwasaki</name></author><author><name sortKey="Urasaki, Y" uniqKey="Urasaki Y">Y. Urasaki</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>France</li></country></list><tree><country name="France"><noRegion><name sortKey="Grassin Delyle, Stanislas" sort="Grassin Delyle, Stanislas" uniqKey="Grassin Delyle S" first="Stanislas" last="Grassin-Delyle">Stanislas Grassin-Delyle</name></noRegion><name sortKey="Abrial, Charlotte" sort="Abrial, Charlotte" uniqKey="Abrial C" first="Charlotte" last="Abrial">Charlotte Abrial</name><name sortKey="Brollo, Marion" sort="Brollo, Marion" uniqKey="Brollo M" first="Marion" last="Brollo">Marion Brollo</name><name sortKey="Couderc, Louis Jean" sort="Couderc, Louis Jean" uniqKey="Couderc L" first="Louis-Jean" last="Couderc">Louis-Jean Couderc</name><name sortKey="Couderc, Louis Jean" sort="Couderc, Louis Jean" uniqKey="Couderc L" first="Louis-Jean" last="Couderc">Louis-Jean Couderc</name><name sortKey="Devillier, Philippe" sort="Devillier, Philippe" uniqKey="Devillier P" first="Philippe" last="Devillier">Philippe Devillier</name><name sortKey="Devillier, Philippe" sort="Devillier, Philippe" uniqKey="Devillier P" first="Philippe" last="Devillier">Philippe Devillier</name><name sortKey="Faisy, Christophe" sort="Faisy, Christophe" uniqKey="Faisy C" first="Christophe" last="Faisy">Christophe Faisy</name><name sortKey="Grassin Delyle, Stanislas" sort="Grassin Delyle, Stanislas" uniqKey="Grassin Delyle S" first="Stanislas" last="Grassin-Delyle">Stanislas Grassin-Delyle</name><name sortKey="Mantov, Nikola" sort="Mantov, Nikola" uniqKey="Mantov N" first="Nikola" last="Mantov">Nikola Mantov</name><name sortKey="Naline, Emmanuel" sort="Naline, Emmanuel" uniqKey="Naline E" first="Emmanuel" last="Naline">Emmanuel Naline</name><name sortKey="Naline, Emmanuel" sort="Naline, Emmanuel" uniqKey="Naline E" first="Emmanuel" last="Naline">Emmanuel Naline</name><name sortKey="Salvator, Helene" sort="Salvator, Helene" uniqKey="Salvator H" first="Hélène" last="Salvator">Hélène Salvator</name><name sortKey="Salvator, Helene" sort="Salvator, Helene" uniqKey="Salvator H" first="Hélène" last="Salvator">Hélène Salvator</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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