Prostaglandin E2 Prevents Hyperosmolar-Induced Human Mast Cell Activation through Prostanoid Receptors EP2 and EP4

Background: Mast cells play a critical role in allergic and inflammatory diseases, including exercise-induced bronchoconstriction (EIB) in asthma. The mechanism underlying EIB is probably related to increased airway fluid osmolarity that activates mast cells to the release inflammatory mediators. Th...

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Autores: Torres Atencio, Ivonne Marisol, Ainsua-Enrich, Erola|||0000-0001-7901-5798, Mora Pérez, Fernando de|||0000-0002-3002-6004, Picado Valles, César, Martín Castillo, Margarita|||0000-0003-4370-6700
Tipo de recurso: artículo
Fecha de publicación:2014
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:141319
Acceso en línea:https://ddd.uab.cat/record/141319
https://dx.doi.org/urn:doi:10.1371/journal.pone.0110870
Access Level:acceso abierto
Palabra clave:Asthma
Inflammatory diseases
MAPK signaling cascades
Mannitol
Mast cells
Phosphorylation
Polymerase chain reaction
Prostaglandin
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spelling Prostaglandin E2 Prevents Hyperosmolar-Induced Human Mast Cell Activation through Prostanoid Receptors EP2 and EP4Torres Atencio, Ivonne MarisolAinsua-Enrich, Erola|||0000-0001-7901-5798Mora Pérez, Fernando de|||0000-0002-3002-6004Picado Valles, CésarMartín Castillo, Margarita|||0000-0003-4370-6700AsthmaInflammatory diseasesMAPK signaling cascadesMannitolMast cellsPhosphorylationPolymerase chain reactionProstaglandinBackground: Mast cells play a critical role in allergic and inflammatory diseases, including exercise-induced bronchoconstriction (EIB) in asthma. The mechanism underlying EIB is probably related to increased airway fluid osmolarity that activates mast cells to the release inflammatory mediators. These mediators then act on bronchial smooth muscle to cause bronchoconstriction. In parallel, protective substances such as prostaglandin E2 (PGE2) are probably also released and could explain the refractory period observed in patients with EIB. Objective: This study aimed to evaluate the protective effect of PGE2 on osmotically activated mast cells, as a model of exercise-induced bronchoconstriction. Methods: We used LAD2, HMC-1, CD34-positive, and human lung mast cell lines. Cells underwent a mannitol challenge, and the effects of PGE2 and prostanoid receptor (EP) antagonists for EP1-4 were assayed on the activated mast cells. Beta-hexosaminidase release, protein phosphorylation, and calcium mobilization were assessed. Results: Mannitol both induced mast cell degranulation and activated phosphatidyl inositide 3-kinase and mitogen-activated protein kinase (MAPK) pathways, thereby causing de novo eicosanoid and cytokine synthesis. The addition of PGE2 significantly reduced mannitol-induced degranulation through EP2 and EP4 receptors, as measured by beta-hexosaminidase release, and consequently calcium influx. Extracellular-signal-regulated kinase 1/2, c-Jun N-terminal kinase, and p38 phosphorylation were diminished when compared with mannitol activation alone. Conclusions:Our data show a protective role for the PGE2 receptors EP2 and EP4 following osmotic changes, through the reduction of human mast cell activity caused by calcium influx impairment and MAP kinase inhibition. 22014-01-0120142014-01-01Articlehttp://purl.org/coar/resource_type/c_6501VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttps://ddd.uab.cat/record/141319https://dx.doi.org/urn:doi:10.1371/journal.pone.0110870reponame:Dipòsit Digital de Documents de la UABinstname:Universitat Autònoma de BarcelonaInglésengopen accesshttp://purl.org/coar/access_right/c_abf2Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.https://creativecommons.org/licenses/by/3.0/info:eu-repo/semantics/openAccessoai:ddd.uab.cat:1413192026-06-06T12:50:31Z
dc.title.none.fl_str_mv Prostaglandin E2 Prevents Hyperosmolar-Induced Human Mast Cell Activation through Prostanoid Receptors EP2 and EP4
title Prostaglandin E2 Prevents Hyperosmolar-Induced Human Mast Cell Activation through Prostanoid Receptors EP2 and EP4
spellingShingle Prostaglandin E2 Prevents Hyperosmolar-Induced Human Mast Cell Activation through Prostanoid Receptors EP2 and EP4
Torres Atencio, Ivonne Marisol
Asthma
Inflammatory diseases
MAPK signaling cascades
Mannitol
Mast cells
Phosphorylation
Polymerase chain reaction
Prostaglandin
title_short Prostaglandin E2 Prevents Hyperosmolar-Induced Human Mast Cell Activation through Prostanoid Receptors EP2 and EP4
title_full Prostaglandin E2 Prevents Hyperosmolar-Induced Human Mast Cell Activation through Prostanoid Receptors EP2 and EP4
title_fullStr Prostaglandin E2 Prevents Hyperosmolar-Induced Human Mast Cell Activation through Prostanoid Receptors EP2 and EP4
title_full_unstemmed Prostaglandin E2 Prevents Hyperosmolar-Induced Human Mast Cell Activation through Prostanoid Receptors EP2 and EP4
title_sort Prostaglandin E2 Prevents Hyperosmolar-Induced Human Mast Cell Activation through Prostanoid Receptors EP2 and EP4
dc.creator.none.fl_str_mv Torres Atencio, Ivonne Marisol
Ainsua-Enrich, Erola|||0000-0001-7901-5798
Mora Pérez, Fernando de|||0000-0002-3002-6004
Picado Valles, César
Martín Castillo, Margarita|||0000-0003-4370-6700
author Torres Atencio, Ivonne Marisol
author_facet Torres Atencio, Ivonne Marisol
Ainsua-Enrich, Erola|||0000-0001-7901-5798
Mora Pérez, Fernando de|||0000-0002-3002-6004
Picado Valles, César
Martín Castillo, Margarita|||0000-0003-4370-6700
author_role author
author2 Ainsua-Enrich, Erola|||0000-0001-7901-5798
Mora Pérez, Fernando de|||0000-0002-3002-6004
Picado Valles, César
Martín Castillo, Margarita|||0000-0003-4370-6700
author2_role author
author
author
author
dc.subject.none.fl_str_mv Asthma
Inflammatory diseases
MAPK signaling cascades
Mannitol
Mast cells
Phosphorylation
Polymerase chain reaction
Prostaglandin
topic Asthma
Inflammatory diseases
MAPK signaling cascades
Mannitol
Mast cells
Phosphorylation
Polymerase chain reaction
Prostaglandin
description Background: Mast cells play a critical role in allergic and inflammatory diseases, including exercise-induced bronchoconstriction (EIB) in asthma. The mechanism underlying EIB is probably related to increased airway fluid osmolarity that activates mast cells to the release inflammatory mediators. These mediators then act on bronchial smooth muscle to cause bronchoconstriction. In parallel, protective substances such as prostaglandin E2 (PGE2) are probably also released and could explain the refractory period observed in patients with EIB. Objective: This study aimed to evaluate the protective effect of PGE2 on osmotically activated mast cells, as a model of exercise-induced bronchoconstriction. Methods: We used LAD2, HMC-1, CD34-positive, and human lung mast cell lines. Cells underwent a mannitol challenge, and the effects of PGE2 and prostanoid receptor (EP) antagonists for EP1-4 were assayed on the activated mast cells. Beta-hexosaminidase release, protein phosphorylation, and calcium mobilization were assessed. Results: Mannitol both induced mast cell degranulation and activated phosphatidyl inositide 3-kinase and mitogen-activated protein kinase (MAPK) pathways, thereby causing de novo eicosanoid and cytokine synthesis. The addition of PGE2 significantly reduced mannitol-induced degranulation through EP2 and EP4 receptors, as measured by beta-hexosaminidase release, and consequently calcium influx. Extracellular-signal-regulated kinase 1/2, c-Jun N-terminal kinase, and p38 phosphorylation were diminished when compared with mannitol activation alone. Conclusions:Our data show a protective role for the PGE2 receptors EP2 and EP4 following osmotic changes, through the reduction of human mast cell activity caused by calcium influx impairment and MAP kinase inhibition.
publishDate 2014
dc.date.none.fl_str_mv 2
2014-01-01
2014
2014-01-01
dc.type.none.fl_str_mv Article
http://purl.org/coar/resource_type/c_6501
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://ddd.uab.cat/record/141319
https://dx.doi.org/urn:doi:10.1371/journal.pone.0110870
url https://ddd.uab.cat/record/141319
https://dx.doi.org/urn:doi:10.1371/journal.pone.0110870
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
https://creativecommons.org/licenses/by/3.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
https://creativecommons.org/licenses/by/3.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:Dipòsit Digital de Documents de la UAB
instname:Universitat Autònoma de Barcelona
instname_str Universitat Autònoma de Barcelona
reponame_str Dipòsit Digital de Documents de la UAB
collection Dipòsit Digital de Documents de la UAB
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