Cyclooxygenase-2 and prostaglandin E2 signaling through prostaglandin receptor EP- 2 favor the development of myocarditis during acute trypanosoma cruzi infection

Inflammation plays an important role in the pathophysiology of Chagas disease, caused by Trypanosoma cruzi. Prostanoids are regulators of homeostasis and inflammation and are produced mainly by myeloid cells, being cyclooxygenases, COX-1 and COX-2, the key enzymes in their biosynthesis from arachido...

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Autores: Guerrero, Néstor A., Camacho, Mercedes|||0000-0001-5970-3294, Vila, Luis|||0000-0003-0150-6129, Íñiguez, Miguel A., Chillón-Marinas, Carlos, Cuervo, Henar, Poveda, Cristina, Fresno, Manuel, Gironès, Núria
Tipo de recurso: artículo
Fecha de publicación:2015
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:299426
Acceso en línea:https://ddd.uab.cat/record/299426
https://dx.doi.org/urn:doi:10.1371/journal.pntd.0004025
Access Level:acceso abierto
Palabra clave:Animals
Chagas Disease
Cyclooxygenase 2
Cytokines
Dinoprostone
Humans
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Myocarditis
Myocardium
Receptors, Prostaglandin E, EP2 Subtype
Trypanosoma cruzi
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spelling Cyclooxygenase-2 and prostaglandin E2 signaling through prostaglandin receptor EP- 2 favor the development of myocarditis during acute trypanosoma cruzi infectionGuerrero, Néstor A.Camacho, Mercedes|||0000-0001-5970-3294Vila, Luis|||0000-0003-0150-6129Íñiguez, Miguel A.Chillón-Marinas, CarlosCuervo, HenarPoveda, CristinaFresno, ManuelGironès, NúriaAnimalsChagas DiseaseCyclooxygenase 2CytokinesDinoprostoneHumansMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMyocarditisMyocardiumReceptors, Prostaglandin E, EP2 SubtypeTrypanosoma cruziInflammation plays an important role in the pathophysiology of Chagas disease, caused by Trypanosoma cruzi. Prostanoids are regulators of homeostasis and inflammation and are produced mainly by myeloid cells, being cyclooxygenases, COX-1 and COX-2, the key enzymes in their biosynthesis from arachidonic acid (AA). Here, we have investigated the expression of enzymes involved in AA metabolism during T. cruzi infection. Our results show an increase in the expression of several of these enzymes in acute T. cruzi infected heart. Interestingly, COX-2 was expressed by CD68 myeloid heart-infiltrating cells. In addition, infiltrating myeloid CD11bLy6G cells purified from infected heart tissue express COX-2 and produce prostaglandin E (PGE) ex vivo. T. cruzi infections in COX-2 or PGE- dependent prostaglandin receptor EP-2 deficient mice indicate that both, COX-2 and EP-2 signaling contribute significantly to the heart leukocyte infiltration and to the release of chemokines and inflammatory cytokines in the heart of T. cruzi infected mice. In conclusion, COX-2 plays a detrimental role in acute Chagas disease myocarditis and points to COX-2 as a potential target for immune intervention.Universitat Autònoma de Barcelona 22015-01-0120152015-01-01Articlehttp://purl.org/coar/resource_type/c_6501VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttps://ddd.uab.cat/record/299426https://dx.doi.org/urn:doi:10.1371/journal.pntd.0004025reponame:Dipòsit Digital de Documents de la UABinstname:Universitat Autònoma de BarcelonaInglésengMinisterio de Ciencia e Innovación https://doi.org/10.13039/501100004837 PS09/00538open 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/4.0/info:eu-repo/semantics/openAccessoai:ddd.uab.cat:2994262026-06-06T12:50:31Z
dc.title.none.fl_str_mv Cyclooxygenase-2 and prostaglandin E2 signaling through prostaglandin receptor EP- 2 favor the development of myocarditis during acute trypanosoma cruzi infection
title Cyclooxygenase-2 and prostaglandin E2 signaling through prostaglandin receptor EP- 2 favor the development of myocarditis during acute trypanosoma cruzi infection
spellingShingle Cyclooxygenase-2 and prostaglandin E2 signaling through prostaglandin receptor EP- 2 favor the development of myocarditis during acute trypanosoma cruzi infection
Guerrero, Néstor A.
Animals
Chagas Disease
Cyclooxygenase 2
Cytokines
Dinoprostone
Humans
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Myocarditis
Myocardium
Receptors, Prostaglandin E, EP2 Subtype
Trypanosoma cruzi
title_short Cyclooxygenase-2 and prostaglandin E2 signaling through prostaglandin receptor EP- 2 favor the development of myocarditis during acute trypanosoma cruzi infection
title_full Cyclooxygenase-2 and prostaglandin E2 signaling through prostaglandin receptor EP- 2 favor the development of myocarditis during acute trypanosoma cruzi infection
title_fullStr Cyclooxygenase-2 and prostaglandin E2 signaling through prostaglandin receptor EP- 2 favor the development of myocarditis during acute trypanosoma cruzi infection
title_full_unstemmed Cyclooxygenase-2 and prostaglandin E2 signaling through prostaglandin receptor EP- 2 favor the development of myocarditis during acute trypanosoma cruzi infection
title_sort Cyclooxygenase-2 and prostaglandin E2 signaling through prostaglandin receptor EP- 2 favor the development of myocarditis during acute trypanosoma cruzi infection
dc.creator.none.fl_str_mv Guerrero, Néstor A.
Camacho, Mercedes|||0000-0001-5970-3294
Vila, Luis|||0000-0003-0150-6129
Íñiguez, Miguel A.
Chillón-Marinas, Carlos
Cuervo, Henar
Poveda, Cristina
Fresno, Manuel
Gironès, Núria
author Guerrero, Néstor A.
author_facet Guerrero, Néstor A.
Camacho, Mercedes|||0000-0001-5970-3294
Vila, Luis|||0000-0003-0150-6129
Íñiguez, Miguel A.
Chillón-Marinas, Carlos
Cuervo, Henar
Poveda, Cristina
Fresno, Manuel
Gironès, Núria
author_role author
author2 Camacho, Mercedes|||0000-0001-5970-3294
Vila, Luis|||0000-0003-0150-6129
Íñiguez, Miguel A.
Chillón-Marinas, Carlos
Cuervo, Henar
Poveda, Cristina
Fresno, Manuel
Gironès, Núria
author2_role author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universitat Autònoma de Barcelona
dc.subject.none.fl_str_mv Animals
Chagas Disease
Cyclooxygenase 2
Cytokines
Dinoprostone
Humans
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Myocarditis
Myocardium
Receptors, Prostaglandin E, EP2 Subtype
Trypanosoma cruzi
topic Animals
Chagas Disease
Cyclooxygenase 2
Cytokines
Dinoprostone
Humans
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Myocarditis
Myocardium
Receptors, Prostaglandin E, EP2 Subtype
Trypanosoma cruzi
description Inflammation plays an important role in the pathophysiology of Chagas disease, caused by Trypanosoma cruzi. Prostanoids are regulators of homeostasis and inflammation and are produced mainly by myeloid cells, being cyclooxygenases, COX-1 and COX-2, the key enzymes in their biosynthesis from arachidonic acid (AA). Here, we have investigated the expression of enzymes involved in AA metabolism during T. cruzi infection. Our results show an increase in the expression of several of these enzymes in acute T. cruzi infected heart. Interestingly, COX-2 was expressed by CD68 myeloid heart-infiltrating cells. In addition, infiltrating myeloid CD11bLy6G cells purified from infected heart tissue express COX-2 and produce prostaglandin E (PGE) ex vivo. T. cruzi infections in COX-2 or PGE- dependent prostaglandin receptor EP-2 deficient mice indicate that both, COX-2 and EP-2 signaling contribute significantly to the heart leukocyte infiltration and to the release of chemokines and inflammatory cytokines in the heart of T. cruzi infected mice. In conclusion, COX-2 plays a detrimental role in acute Chagas disease myocarditis and points to COX-2 as a potential target for immune intervention.
publishDate 2015
dc.date.none.fl_str_mv 2
2015-01-01
2015
2015-01-01
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/299426
https://dx.doi.org/urn:doi:10.1371/journal.pntd.0004025
url https://ddd.uab.cat/record/299426
https://dx.doi.org/urn:doi:10.1371/journal.pntd.0004025
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.relation.none.fl_str_mv Ministerio de Ciencia e Innovación https://doi.org/10.13039/501100004837 PS09/00538
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
https://creativecommons.org/licenses/by/4.0/
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/4.0/
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
repository.name.fl_str_mv
repository.mail.fl_str_mv
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