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Bitter Taste Receptor Agonists Mitigate Features of Allergic Asthma in Mice.

Identifieur interne : 000179 ( PubMed/Checkpoint ); précédent : 000178; suivant : 000180

Bitter Taste Receptor Agonists Mitigate Features of Allergic Asthma in Mice.

Auteurs : Pawan Sharma [États-Unis] ; Roslyn Yi [États-Unis] ; Ajay P. Nayak [États-Unis] ; Nadan Wang [États-Unis] ; Francesca Tang [Australie] ; Morgan J. Knight [États-Unis] ; Shi Pan [États-Unis] ; Brian Oliver [Australie] ; Deepak A. Deshpande [États-Unis]

Source :

RBID : pubmed:28397820

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Abstract

Asthma is characterized by airway inflammation, mucus secretion, remodeling and hyperresponsiveness (AHR). Recent research has established the bronchodilatory effect of bitter taste receptor (TAS2R) agonists in various models. Comprehensive pre-clinical studies aimed at establishing effectiveness of TAS2R agonists in disease models are lacking. Here we aimed to determine the effect of TAS2R agonists on features of asthma. Further, we elucidated a mechanism by which TAS2R agonists mitigate features of asthma. Asthma was induced in mice using intranasal house dust mite or aerosol ova-albumin challenge, and chloroquine or quinine were tested in both prophylactic and treatment models. Allergen challenge resulted in airway inflammation as evidenced by increased immune cells infiltration and release of cytokines and chemokines in the lungs, which were significantly attenuated in TAS2R agonists treated mice. TAS2R agonists attenuated features of airway remodeling including smooth muscle mass, extracellular matrix deposition and pro-fibrotic signaling, and also prevented mucus accumulation and development of AHR in mice. Mechanistic studies using human neutrophils demonstrated that inhibition of immune cell chemotaxis is a key mechanism by which TAS2R agonists blocked allergic airway inflammation and exerted anti-asthma effects. Our comprehensive studies establish the effectiveness of TAS2R agonists in mitigating multiple features of allergic asthma.

DOI: 10.1038/srep46166
PubMed: 28397820


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<keywords scheme="KwdEn" xml:lang="en">
<term>Airway Remodeling (drug effects)</term>
<term>Allergens (immunology)</term>
<term>Animals</term>
<term>Asthma (drug therapy)</term>
<term>Asthma (immunology)</term>
<term>Asthma (physiopathology)</term>
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<term>Hypersensitivity (immunology)</term>
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<term>Hypersensitivity (prevention & control)</term>
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<term>Lung (physiopathology)</term>
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<term>Asthme ()</term>
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<term>Asthme (physiopathologie)</term>
<term>Asthme (traitement médicamenteux)</term>
<term>Chimiotaxie ()</term>
<term>Chloroquine (usage thérapeutique)</term>
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<term>Goût</term>
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<term>Hyperréactivité bronchique (physiopathologie)</term>
<term>Hypersensibilité ()</term>
<term>Hypersensibilité (immunologie)</term>
<term>Hypersensibilité (physiopathologie)</term>
<term>Hypersensibilité (traitement médicamenteux)</term>
<term>Immunisation</term>
<term>Inflammation ()</term>
<term>Inflammation (anatomopathologie)</term>
<term>Liquide de lavage bronchoalvéolaire (cytologie)</term>
<term>Matrix metalloproteinases (métabolisme)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mucus (métabolisme)</term>
<term>Muscles lisses ()</term>
<term>Muscles lisses (anatomopathologie)</term>
<term>Numération cellulaire</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (immunologie)</term>
<term>Poumon (parasitologie)</term>
<term>Poumon (physiopathologie)</term>
<term>Pyroglyphidae ()</term>
<term>Quinine (usage thérapeutique)</term>
<term>Remodelage des voies aériennes ()</term>
<term>Récepteurs couplés aux protéines G (agonistes)</term>
<term>Récepteurs couplés aux protéines G (métabolisme)</term>
<term>Souris de lignée BALB C</term>
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<term>Récepteurs couplés aux protéines G</term>
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<term>Hyperréactivité bronchique</term>
<term>Inflammation</term>
<term>Muscles lisses</term>
<term>Poumon</term>
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<term>Bronchial Hyperreactivity</term>
<term>Inflammation</term>
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<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr">
<term>Liquide de lavage bronchoalvéolaire</term>
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<keywords scheme="MESH" qualifier="cytology" xml:lang="en">
<term>Bronchoalveolar Lavage Fluid</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en">
<term>Airway Remodeling</term>
<term>Chemotaxis</term>
<term>Muscle, Smooth</term>
<term>Neutrophils</term>
<term>Pyroglyphidae</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en">
<term>Asthma</term>
<term>Hypersensitivity</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr">
<term>Allergènes</term>
<term>Asthme</term>
<term>Hyperréactivité bronchique</term>
<term>Hypersensibilité</term>
<term>Poumon</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en">
<term>Asthma</term>
<term>Bronchial Hyperreactivity</term>
<term>Hypersensitivity</term>
<term>Lung</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en">
<term>Cytokines</term>
<term>Matrix Metalloproteinases</term>
<term>Mucus</term>
<term>Receptors, G-Protein-Coupled</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>Cytokines</term>
<term>Matrix metalloproteinases</term>
<term>Mucus</term>
<term>Récepteurs couplés aux protéines G</term>
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<term>Poumon</term>
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<keywords scheme="MESH" qualifier="parasitology" xml:lang="en">
<term>Lung</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en">
<term>Bronchial Hyperreactivity</term>
<term>Inflammation</term>
<term>Lung</term>
<term>Muscle, Smooth</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr">
<term>Asthme</term>
<term>Hyperréactivité bronchique</term>
<term>Hypersensibilité</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en">
<term>Asthma</term>
<term>Bronchial Hyperreactivity</term>
<term>Hypersensitivity</term>
<term>Lung</term>
</keywords>
<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en">
<term>Asthma</term>
<term>Hypersensitivity</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en">
<term>Chloroquine</term>
<term>Quinine</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr">
<term>Asthme</term>
<term>Hypersensibilité</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr">
<term>Chloroquine</term>
<term>Quinine</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Animals</term>
<term>Cell Count</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Humans</term>
<term>Immunization</term>
<term>Mice, Inbred BALB C</term>
<term>Taste</term>
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<term>Muscles lisses</term>
<term>Numération cellulaire</term>
<term>Pyroglyphidae</term>
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<front>
<div type="abstract" xml:lang="en">Asthma is characterized by airway inflammation, mucus secretion, remodeling and hyperresponsiveness (AHR). Recent research has established the bronchodilatory effect of bitter taste receptor (TAS2R) agonists in various models. Comprehensive pre-clinical studies aimed at establishing effectiveness of TAS2R agonists in disease models are lacking. Here we aimed to determine the effect of TAS2R agonists on features of asthma. Further, we elucidated a mechanism by which TAS2R agonists mitigate features of asthma. Asthma was induced in mice using intranasal house dust mite or aerosol ova-albumin challenge, and chloroquine or quinine were tested in both prophylactic and treatment models. Allergen challenge resulted in airway inflammation as evidenced by increased immune cells infiltration and release of cytokines and chemokines in the lungs, which were significantly attenuated in TAS2R agonists treated mice. TAS2R agonists attenuated features of airway remodeling including smooth muscle mass, extracellular matrix deposition and pro-fibrotic signaling, and also prevented mucus accumulation and development of AHR in mice. Mechanistic studies using human neutrophils demonstrated that inhibition of immune cell chemotaxis is a key mechanism by which TAS2R agonists blocked allergic airway inflammation and exerted anti-asthma effects. Our comprehensive studies establish the effectiveness of TAS2R agonists in mitigating multiple features of allergic asthma.</div>
</front>
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<AbstractText>Asthma is characterized by airway inflammation, mucus secretion, remodeling and hyperresponsiveness (AHR). Recent research has established the bronchodilatory effect of bitter taste receptor (TAS2R) agonists in various models. Comprehensive pre-clinical studies aimed at establishing effectiveness of TAS2R agonists in disease models are lacking. Here we aimed to determine the effect of TAS2R agonists on features of asthma. Further, we elucidated a mechanism by which TAS2R agonists mitigate features of asthma. Asthma was induced in mice using intranasal house dust mite or aerosol ova-albumin challenge, and chloroquine or quinine were tested in both prophylactic and treatment models. Allergen challenge resulted in airway inflammation as evidenced by increased immune cells infiltration and release of cytokines and chemokines in the lungs, which were significantly attenuated in TAS2R agonists treated mice. TAS2R agonists attenuated features of airway remodeling including smooth muscle mass, extracellular matrix deposition and pro-fibrotic signaling, and also prevented mucus accumulation and development of AHR in mice. Mechanistic studies using human neutrophils demonstrated that inhibition of immune cell chemotaxis is a key mechanism by which TAS2R agonists blocked allergic airway inflammation and exerted anti-asthma effects. Our comprehensive studies establish the effectiveness of TAS2R agonists in mitigating multiple features of allergic asthma.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y">
<Author ValidYN="Y">
<LastName>Sharma</LastName>
<ForeName>Pawan</ForeName>
<Initials>P</Initials>
<AffiliationInfo>
<Affiliation>Department of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA, 19107, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Respiratory Research Group, Woolcock Institute of Medical Research and School of Life Sciences, University of Technology, Sydney, NSW, 2007, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Yi</LastName>
<ForeName>Roslyn</ForeName>
<Initials>R</Initials>
<AffiliationInfo>
<Affiliation>Department of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA, 19107, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Nayak</LastName>
<ForeName>Ajay P</ForeName>
<Initials>AP</Initials>
<AffiliationInfo>
<Affiliation>Department of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA, 19107, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Wang</LastName>
<ForeName>Nadan</ForeName>
<Initials>N</Initials>
<AffiliationInfo>
<Affiliation>Department of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA, 19107, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Tang</LastName>
<ForeName>Francesca</ForeName>
<Initials>F</Initials>
<AffiliationInfo>
<Affiliation>Respiratory Research Group, Woolcock Institute of Medical Research and School of Life Sciences, University of Technology, Sydney, NSW, 2007, Australia.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Knight</LastName>
<ForeName>Morgan J</ForeName>
<Initials>MJ</Initials>
<AffiliationInfo>
<Affiliation>Department of Experimental Therapeutics, University of Texas MD Anderson Cancer Center, Houston, TX, 77054, USA.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Pan</LastName>
<ForeName>Shi</ForeName>
<Initials>S</Initials>
<AffiliationInfo>
<Affiliation>Department of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA, 19107, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Oliver</LastName>
<ForeName>Brian</ForeName>
<Initials>B</Initials>
<AffiliationInfo>
<Affiliation>Respiratory Research Group, Woolcock Institute of Medical Research and School of Life Sciences, University of Technology, Sydney, NSW, 2007, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Deshpande</LastName>
<ForeName>Deepak A</ForeName>
<Initials>DA</Initials>
<AffiliationInfo>
<Affiliation>Department of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA, 19107, USA.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList>
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<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic">
<Year>2017</Year>
<Month>04</Month>
<Day>11</Day>
</ArticleDate>
</Article>
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<Country>England</Country>
<MedlineTA>Sci Rep</MedlineTA>
<NlmUniqueID>101563288</NlmUniqueID>
<ISSNLinking>2045-2322</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList>
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<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000485">Allergens</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016207">Cytokines</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D043562">Receptors, G-Protein-Coupled</NameOfSubstance>
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<NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance>
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<NameOfSubstance UI="D011803">Quinine</NameOfSubstance>
</Chemical>
<Chemical>
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</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList>
<MeshHeading>
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<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading>
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<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading>
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<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D016535" MajorTopicYN="N">Bronchial Hyperreactivity</DescriptorName>
<QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D001992" MajorTopicYN="N">Bronchoalveolar Lavage Fluid</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D002452" MajorTopicYN="N">Cell Count</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D002633" MajorTopicYN="N">Chemotaxis</DescriptorName>
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</MeshHeading>
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<DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
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<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
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</MeshHeading>
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<DescriptorName UI="D009093" MajorTopicYN="N">Mucus</DescriptorName>
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