Identification of Epithelial Phospholipase A2 Receptor 1 as a Potential Target in Asthma.
Identifieur interne : 003887 ( Ncbi/Checkpoint ); précédent : 003886; suivant : 003888Identification of Epithelial Phospholipase A2 Receptor 1 as a Potential Target in Asthma.
Auteurs : James D. Nolin ; H Luke Ogden ; Ying Lai ; William A. Altemeier ; Charles W. Frevert ; James G. Bollinger ; Gajendra S. Naika ; Anthony Kicic [Australie] ; Stephen M. Stick [Australie] ; Gerard Lambeau [France] ; William R. Henderson ; Michael H. Gelb ; Teal S. HallstrandSource :
- American journal of respiratory cell and molecular biology [ 1535-4989 ] ; 2016.
Descripteurs français
- KwdFr :
- Allergènes (immunologie), Animaux, Antigènes (immunologie), Asthme (), Asthme (immunologie), Asthme (métabolisme), Asthme (physiopathologie), Cellules épithéliales (anatomopathologie), Cellules épithéliales (métabolisme), Chlorure de méthacholine, Cytokines (biosynthèse), Enfant, Granulocytes éosinophiles (métabolisme), Humains, Immunoglobuline G (métabolisme), Liquide de lavage bronchoalvéolaire, Modèles animaux de maladie humaine, Mucines (métabolisme), Mécanique respiratoire, Pneumopathie infectieuse (anatomopathologie), Pneumopathie infectieuse (métabolisme), Récepteurs à la phospholipase A2 (déficit), Récepteurs à la phospholipase A2 (génétique), Récepteurs à la phospholipase A2 (métabolisme), Souris de lignée C57BL, Thérapie moléculaire ciblée, Études de cohortes.
- MESH :
- anatomopathologie : Cellules épithéliales, Pneumopathie infectieuse.
- biosynthèse : Cytokines.
- déficit : Récepteurs à la phospholipase A2.
- génétique : Récepteurs à la phospholipase A2.
- immunologie : Allergènes, Antigènes, Asthme.
- métabolisme : Asthme, Cellules épithéliales, Granulocytes éosinophiles, Immunoglobuline G, Mucines, Pneumopathie infectieuse, Récepteurs à la phospholipase A2.
- physiopathologie : Asthme.
- Animaux, Asthme, Chlorure de méthacholine, Enfant, Humains, Liquide de lavage bronchoalvéolaire, Modèles animaux de maladie humaine, Mécanique respiratoire, Souris de lignée C57BL, Thérapie moléculaire ciblée, Études de cohortes.
English descriptors
- KwdEn :
- Allergens (immunology), Animals, Antigens (immunology), Asthma (immunology), Asthma (metabolism), Asthma (physiopathology), Asthma (therapy), Bronchoalveolar Lavage Fluid, Child, Cohort Studies, Cytokines (biosynthesis), Disease Models, Animal, Eosinophils (metabolism), Epithelial Cells (metabolism), Epithelial Cells (pathology), Humans, Immunoglobulin G (metabolism), Methacholine Chloride, Mice, Inbred C57BL, Molecular Targeted Therapy, Mucins (metabolism), Pneumonia (metabolism), Pneumonia (pathology), Receptors, Phospholipase A2 (deficiency), Receptors, Phospholipase A2 (genetics), Receptors, Phospholipase A2 (metabolism), Respiratory Mechanics.
- MESH :
- chemical , biosynthesis : Cytokines.
- chemical , deficiency : Receptors, Phospholipase A2.
- chemical , genetics : Receptors, Phospholipase A2.
- chemical , immunology : Allergens, Antigens.
- immunology : Asthma.
- metabolism : Asthma, Eosinophils, Epithelial Cells, Immunoglobulin G, Mucins, Pneumonia, Receptors, Phospholipase A2.
- pathology : Epithelial Cells, Pneumonia.
- physiopathology : Asthma.
- therapy : Asthma.
- Animals, Bronchoalveolar Lavage Fluid, Child, Cohort Studies, Disease Models, Animal, Humans, Methacholine Chloride, Mice, Inbred C57BL, Molecular Targeted Therapy, Respiratory Mechanics.
Abstract
Secreted phospholipase A2s (sPLA2s) regulate eicosanoid formation and have been implicated in asthma. Although sPLA2s function as enzymes, some of the sPLA2s bind with high affinity to a C-type lectin receptor, called PLA2R1, which has functions in both cellular signaling and clearance of sPLA2s. We sought to examine the expression of PLA2R1 in the airway epithelium of human subjects with asthma and the function of the murine Pla2r1 gene in a model of asthma. Expression of PLA2R1 in epithelial brushings was assessed in two distinct cohorts of children with asthma by microarray and quantitative PCR, and immunostaining for PLA2R1 was conducted on endobronchial tissue and epithelial brushings from adults with asthma. C57BL/129 mice deficient in Pla2r1 (Pla2r1(-/-)) were characterized in an ovalbumin (OVA) model of allergic asthma. PLA2R1 was differentially overexpressed in epithelial brushings of children with atopic asthma in both cohorts. Immunostaining for PLA2R1 in endobronchial tissue localized to submucosal glandular epithelium and columnar epithelial cells. After OVA sensitization and challenge, Pla2r1(-/-) mice had increased airway hyperresponsiveness, as well as an increase in cellular trafficking of eosinophils to the peribronchial space and bronchoalveolar lavage fluid, and an increase in airway permeability. In addition, Pla2r1(-/-) mice had more dendritic cells in the lung, higher levels of OVA-specific IgG, and increased production of both type-1 and type-2 cytokines by lung leukocytes. PLA2R1 is increased in the airway epithelium in asthma, and serves as a regulator of airway hyperresponsiveness, airway permeability, antigen sensitization, and airway inflammation.
DOI: 10.1165/rcmb.2015-0150OC
PubMed: 27448109
Affiliations:
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Nolin</name><affiliation><nlm:affiliation>From the 1 Division of Pulmonary and Critical Care and.</nlm:affiliation><wicri:noCountry code="no comma">From the 1 Division of Pulmonary and Critical Care and.</wicri:noCountry></affiliation></author><author><name sortKey="Ogden, H Luke" sort="Ogden, H Luke" uniqKey="Ogden H" first="H Luke" last="Ogden">H Luke Ogden</name><affiliation><nlm:affiliation>From the 1 Division of Pulmonary and Critical Care and.</nlm:affiliation><wicri:noCountry code="no comma">From the 1 Division of Pulmonary and Critical Care and.</wicri:noCountry></affiliation></author><author><name sortKey="Lai, Ying" sort="Lai, Ying" uniqKey="Lai Y" first="Ying" last="Lai">Ying Lai</name><affiliation><nlm:affiliation>From the 1 Division of Pulmonary and Critical Care and.</nlm:affiliation><wicri:noCountry code="no comma">From the 1 Division of Pulmonary and Critical Care and.</wicri:noCountry></affiliation></author><author><name sortKey="Altemeier, William A" sort="Altemeier, William A" uniqKey="Altemeier W" first="William A" last="Altemeier">William A. Altemeier</name><affiliation><nlm:affiliation>From the 1 Division of Pulmonary and Critical Care and.</nlm:affiliation><wicri:noCountry code="no comma">From the 1 Division of Pulmonary and Critical Care and.</wicri:noCountry></affiliation></author><author><name sortKey="Frevert, Charles W" sort="Frevert, Charles W" uniqKey="Frevert C" first="Charles W" last="Frevert">Charles W. Frevert</name><affiliation><nlm:affiliation>From the 1 Division of Pulmonary and Critical Care and.</nlm:affiliation><wicri:noCountry code="no comma">From the 1 Division of Pulmonary and Critical Care and.</wicri:noCountry></affiliation></author><author><name sortKey="Bollinger, James G" sort="Bollinger, James G" uniqKey="Bollinger J" first="James G" last="Bollinger">James G. Bollinger</name><affiliation><nlm:affiliation>3 Department of Chemistry, and.</nlm:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Naika, Gajendra S" sort="Naika, Gajendra S" uniqKey="Naika G" first="Gajendra S" last="Naika">Gajendra S. Naika</name><affiliation><nlm:affiliation>3 Department of Chemistry, and.</nlm:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Kicic, Anthony" sort="Kicic, Anthony" uniqKey="Kicic A" first="Anthony" last="Kicic">Anthony Kicic</name><affiliation wicri:level="1"><nlm:affiliation>4 The Telethon Kids Institute, Centre for Health Research, University of Western Australia, Nedlands, Western Australia, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>4 The Telethon Kids Institute, Centre for Health Research, University of Western Australia, Nedlands, Western Australia</wicri:regionArea><wicri:noRegion>Western Australia</wicri:noRegion></affiliation></author><author><name sortKey="Stick, Stephen M" sort="Stick, Stephen M" uniqKey="Stick S" first="Stephen M" last="Stick">Stephen M. Stick</name><affiliation wicri:level="1"><nlm:affiliation>4 The Telethon Kids Institute, Centre for Health Research, University of Western Australia, Nedlands, Western Australia, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>4 The Telethon Kids Institute, Centre for Health Research, University of Western Australia, Nedlands, Western Australia</wicri:regionArea><wicri:noRegion>Western Australia</wicri:noRegion></affiliation></author><author><name sortKey="Lambeau, Gerard" sort="Lambeau, Gerard" uniqKey="Lambeau G" first="Gerard" last="Lambeau">Gerard Lambeau</name><affiliation wicri:level="1"><nlm:affiliation>8 Institut de Pharmacologie Moléculaire et Cellulaire, Valbonne, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>8 Institut de Pharmacologie Moléculaire et Cellulaire, Valbonne</wicri:regionArea><wicri:noRegion>Valbonne</wicri:noRegion><wicri:noRegion>Valbonne</wicri:noRegion></affiliation></author><author><name sortKey="Henderson, William R" sort="Henderson, William R" uniqKey="Henderson W" first="William R" last="Henderson">William R. Henderson</name><affiliation><nlm:affiliation>9 Division of Allergy and Infectious Diseases, Department of Medicine, and.</nlm:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Gelb, Michael H" sort="Gelb, Michael H" uniqKey="Gelb M" first="Michael H" last="Gelb">Michael H. Gelb</name><affiliation><nlm:affiliation>3 Department of Chemistry, and.</nlm:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Hallstrand, Teal S" sort="Hallstrand, Teal S" uniqKey="Hallstrand T" first="Teal S" last="Hallstrand">Teal S. Hallstrand</name><affiliation><nlm:affiliation>From the 1 Division of Pulmonary and Critical Care and.</nlm:affiliation><wicri:noCountry code="no comma">From the 1 Division of Pulmonary and Critical Care and.</wicri:noCountry></affiliation></author></analytic><series><title level="j">American journal of respiratory cell and molecular biology</title><idno type="eISSN">1535-4989</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Allergens (immunology)</term><term>Animals</term><term>Antigens (immunology)</term><term>Asthma (immunology)</term><term>Asthma (metabolism)</term><term>Asthma (physiopathology)</term><term>Asthma (therapy)</term><term>Bronchoalveolar Lavage Fluid</term><term>Child</term><term>Cohort Studies</term><term>Cytokines (biosynthesis)</term><term>Disease Models, Animal</term><term>Eosinophils (metabolism)</term><term>Epithelial Cells (metabolism)</term><term>Epithelial Cells (pathology)</term><term>Humans</term><term>Immunoglobulin G (metabolism)</term><term>Methacholine Chloride</term><term>Mice, Inbred C57BL</term><term>Molecular Targeted Therapy</term><term>Mucins (metabolism)</term><term>Pneumonia (metabolism)</term><term>Pneumonia (pathology)</term><term>Receptors, Phospholipase A2 (deficiency)</term><term>Receptors, Phospholipase A2 (genetics)</term><term>Receptors, Phospholipase A2 (metabolism)</term><term>Respiratory Mechanics</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Allergènes (immunologie)</term><term>Animaux</term><term>Antigènes (immunologie)</term><term>Asthme ()</term><term>Asthme (immunologie)</term><term>Asthme (métabolisme)</term><term>Asthme (physiopathologie)</term><term>Cellules épithéliales (anatomopathologie)</term><term>Cellules épithéliales (métabolisme)</term><term>Chlorure de méthacholine</term><term>Cytokines (biosynthèse)</term><term>Enfant</term><term>Granulocytes éosinophiles (métabolisme)</term><term>Humains</term><term>Immunoglobuline G (métabolisme)</term><term>Liquide de lavage bronchoalvéolaire</term><term>Modèles animaux de maladie humaine</term><term>Mucines (métabolisme)</term><term>Mécanique respiratoire</term><term>Pneumopathie infectieuse (anatomopathologie)</term><term>Pneumopathie infectieuse (métabolisme)</term><term>Récepteurs à la phospholipase A2 (déficit)</term><term>Récepteurs à la phospholipase A2 (génétique)</term><term>Récepteurs à la phospholipase A2 (métabolisme)</term><term>Souris de lignée C57BL</term><term>Thérapie moléculaire ciblée</term><term>Études de cohortes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Receptors, Phospholipase A2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, Phospholipase A2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Allergens</term><term>Antigens</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cellules épithéliales</term><term>Pneumopathie infectieuse</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Récepteurs à la phospholipase A2</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Récepteurs à la phospholipase A2</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Allergènes</term><term>Antigènes</term><term>Asthme</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Asthma</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Asthma</term><term>Eosinophils</term><term>Epithelial Cells</term><term>Immunoglobulin G</term><term>Mucins</term><term>Pneumonia</term><term>Receptors, Phospholipase A2</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Asthme</term><term>Cellules épithéliales</term><term>Granulocytes éosinophiles</term><term>Immunoglobuline G</term><term>Mucines</term><term>Pneumopathie infectieuse</term><term>Récepteurs à la phospholipase A2</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Epithelial Cells</term><term>Pneumonia</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Asthme</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Asthma</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Asthma</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Bronchoalveolar Lavage Fluid</term><term>Child</term><term>Cohort Studies</term><term>Disease Models, Animal</term><term>Humans</term><term>Methacholine Chloride</term><term>Mice, Inbred C57BL</term><term>Molecular Targeted Therapy</term><term>Respiratory Mechanics</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Asthme</term><term>Chlorure de méthacholine</term><term>Enfant</term><term>Humains</term><term>Liquide de lavage bronchoalvéolaire</term><term>Modèles animaux de maladie humaine</term><term>Mécanique respiratoire</term><term>Souris de lignée C57BL</term><term>Thérapie moléculaire ciblée</term><term>Études de cohortes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Secreted phospholipase A2s (sPLA2s) regulate eicosanoid formation and have been implicated in asthma. Although sPLA2s function as enzymes, some of the sPLA2s bind with high affinity to a C-type lectin receptor, called PLA2R1, which has functions in both cellular signaling and clearance of sPLA2s. We sought to examine the expression of PLA2R1 in the airway epithelium of human subjects with asthma and the function of the murine Pla2r1 gene in a model of asthma. Expression of PLA2R1 in epithelial brushings was assessed in two distinct cohorts of children with asthma by microarray and quantitative PCR, and immunostaining for PLA2R1 was conducted on endobronchial tissue and epithelial brushings from adults with asthma. C57BL/129 mice deficient in Pla2r1 (Pla2r1(-/-)) were characterized in an ovalbumin (OVA) model of allergic asthma. PLA2R1 was differentially overexpressed in epithelial brushings of children with atopic asthma in both cohorts. Immunostaining for PLA2R1 in endobronchial tissue localized to submucosal glandular epithelium and columnar epithelial cells. After OVA sensitization and challenge, Pla2r1(-/-) mice had increased airway hyperresponsiveness, as well as an increase in cellular trafficking of eosinophils to the peribronchial space and bronchoalveolar lavage fluid, and an increase in airway permeability. In addition, Pla2r1(-/-) mice had more dendritic cells in the lung, higher levels of OVA-specific IgG, and increased production of both type-1 and type-2 cytokines by lung leukocytes. PLA2R1 is increased in the airway epithelium in asthma, and serves as a regulator of airway hyperresponsiveness, airway permeability, antigen sensitization, and airway inflammation.</div></front></TEI><affiliations><list><country><li>Australie</li><li>France</li></country></list><tree><noCountry><name sortKey="Altemeier, William A" sort="Altemeier, William A" uniqKey="Altemeier W" first="William A" last="Altemeier">William A. Altemeier</name><name sortKey="Bollinger, James G" sort="Bollinger, James G" uniqKey="Bollinger J" first="James G" last="Bollinger">James G. Bollinger</name><name sortKey="Frevert, Charles W" sort="Frevert, Charles W" uniqKey="Frevert C" first="Charles W" last="Frevert">Charles W. Frevert</name><name sortKey="Gelb, Michael H" sort="Gelb, Michael H" uniqKey="Gelb M" first="Michael H" last="Gelb">Michael H. Gelb</name><name sortKey="Hallstrand, Teal S" sort="Hallstrand, Teal S" uniqKey="Hallstrand T" first="Teal S" last="Hallstrand">Teal S. Hallstrand</name><name sortKey="Henderson, William R" sort="Henderson, William R" uniqKey="Henderson W" first="William R" last="Henderson">William R. Henderson</name><name sortKey="Lai, Ying" sort="Lai, Ying" uniqKey="Lai Y" first="Ying" last="Lai">Ying Lai</name><name sortKey="Naika, Gajendra S" sort="Naika, Gajendra S" uniqKey="Naika G" first="Gajendra S" last="Naika">Gajendra S. Naika</name><name sortKey="Nolin, James D" sort="Nolin, James D" uniqKey="Nolin J" first="James D" last="Nolin">James D. Nolin</name><name sortKey="Ogden, H Luke" sort="Ogden, H Luke" uniqKey="Ogden H" first="H Luke" last="Ogden">H Luke Ogden</name></noCountry><country name="Australie"><noRegion><name sortKey="Kicic, Anthony" sort="Kicic, Anthony" uniqKey="Kicic A" first="Anthony" last="Kicic">Anthony Kicic</name></noRegion><name sortKey="Stick, Stephen M" sort="Stick, Stephen M" uniqKey="Stick S" first="Stephen M" last="Stick">Stephen M. Stick</name></country><country name="France"><noRegion><name sortKey="Lambeau, Gerard" sort="Lambeau, Gerard" uniqKey="Lambeau G" first="Gerard" last="Lambeau">Gerard Lambeau</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Identification of Epithelial Phospholipase A2 Receptor 1 as a Potential Target in Asthma.
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Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Ncbi/Checkpoint/RBID.i -Sk "pubmed:27448109" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Ncbi/Checkpoint/biblio.hfd \
| NlmPubMed2Wicri -a AustralieFrV1
| This area was generated with Dilib version V0.6.33. |  |