Evidence of eosinophil extracellular trap cell death in copd: Does it represent the trigger that switches on the disease?

Autores
Echevarría, Loli Uribe; Leimgruber, Carolina; García González, Jorge; Nevado, Alberto; Álvarez, Ruth; García, Luciana Noemí; Quintar, Amado Alfredo; Maldonado, Cristina Alicia
Año de publicación
2017
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
In spite of the numerous studies on chronic obstructive pulmonary disease (COPD), the cellular and molecular basis of the disease’s development remain unclear. Neutrophils and eosinophils are known to be key players in COPD. Recently, neutrophil extracellular trap cell death (NETosis), a mechanism due to decondensation and extrusion of chromatin to form extracellular traps, has been demonstrated in COPD. However, there is limited knowledge about eosinophil extracellular trap cell death (EETosis) and its role in the pathogenesis of COPD. The aim of this study was to evaluate EETosis in stable COPD. Induced sputum obtained from healthy smokers and low exacerbation risk COPD A or B group patients or high exacerbation risk COPD C or D group patients were included. Samples were examined using electron microscopy and immunofluorescence. Healthy smokers (n=10) and COPD A (n=19) group exhibited neutrophilic or paucigranulocytic phenotypes, with NETosis being absent in these patients. In contrast, COPD B (n=29), with eosinophilic or mixed phenotypes, showed EETosis and incipient NETosis. COPD C (n=18) and COPD D groups (n=13) were differentiated from low exacerbation rate-COPD group by the abundant cellular debris, with COPD C group having an eosinophilic pattern and numerous cells undergoing EETosis. A hallmark of this group was the abundant released membranes that often appeared phagocytosed by neutrophils, which coincidentally exhibited early NETosis changes. The COPD D group included patients with a neutrophilic or mixed pattern, with abundant neutrophil extracellular trap-derived material. This study is the first to demonstrate EETosis at different stages of stable COPD. The results suggest a role for eosinophils in COPD pathophysiology, especially at the beginning and during the persistence of the disease, regardless of whether the patient quit smoking, with EETosis debris probably triggering uncontrolled NETosis. The main target of these findings should be young smokers with the potential to develop COPD.
Fil: Echevarría, Loli Uribe. Sanatorio Allende; Argentina
Fil: Leimgruber, Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina. Universidad Nacional de Córdoba;Facultad de Ciencias Médicas;Cátedra de Bioquímica Molecular; Argentina
Fil: García González, Jorge. Sanatorio Allende; Argentina
Fil: Nevado, Alberto. Sanatorio Allende; Argentina
Fil: Álvarez, Ruth. Nuevo Hospital San Roque; Argentina
Fil: García, Luciana Noemí. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina. Universidad Nacional de Córdoba;Facultad de Ciencias Médicas;Cátedra de Bioquímica Molecular; Argentina
Fil: Quintar, Amado Alfredo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina. Universidad Nacional de Córdoba;Facultad de Ciencias Médicas;Cátedra de Bioquímica Molecular; Argentina
Fil: Maldonado, Cristina Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina. Universidad Nacional de Córdoba;Facultad de Ciencias Médicas;Cátedra de Bioquímica Molecular; Argentina
Materia
COPD
EETOSIS
EOSINOPHILS
INDUCED SPUTUM
NETOSIS
NEUTROPHILS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/64235
Acceder
id CONICETDig_cf6099891fb4b9ff31bdaf28fd426bbe
oai_identifier_str oai:ri.conicet.gov.ar:11336/64235
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Evidence of eosinophil extracellular trap cell death in copd: Does it represent the trigger that switches on the disease?Echevarría, Loli UribeLeimgruber, CarolinaGarcía González, JorgeNevado, AlbertoÁlvarez, RuthGarcía, Luciana NoemíQuintar, Amado AlfredoMaldonado, Cristina AliciaCOPDEETOSISEOSINOPHILSINDUCED SPUTUMNETOSISNEUTROPHILShttps://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3In spite of the numerous studies on chronic obstructive pulmonary disease (COPD), the cellular and molecular basis of the disease’s development remain unclear. Neutrophils and eosinophils are known to be key players in COPD. Recently, neutrophil extracellular trap cell death (NETosis), a mechanism due to decondensation and extrusion of chromatin to form extracellular traps, has been demonstrated in COPD. However, there is limited knowledge about eosinophil extracellular trap cell death (EETosis) and its role in the pathogenesis of COPD. The aim of this study was to evaluate EETosis in stable COPD. Induced sputum obtained from healthy smokers and low exacerbation risk COPD A or B group patients or high exacerbation risk COPD C or D group patients were included. Samples were examined using electron microscopy and immunofluorescence. Healthy smokers (n=10) and COPD A (n=19) group exhibited neutrophilic or paucigranulocytic phenotypes, with NETosis being absent in these patients. In contrast, COPD B (n=29), with eosinophilic or mixed phenotypes, showed EETosis and incipient NETosis. COPD C (n=18) and COPD D groups (n=13) were differentiated from low exacerbation rate-COPD group by the abundant cellular debris, with COPD C group having an eosinophilic pattern and numerous cells undergoing EETosis. A hallmark of this group was the abundant released membranes that often appeared phagocytosed by neutrophils, which coincidentally exhibited early NETosis changes. The COPD D group included patients with a neutrophilic or mixed pattern, with abundant neutrophil extracellular trap-derived material. This study is the first to demonstrate EETosis at different stages of stable COPD. The results suggest a role for eosinophils in COPD pathophysiology, especially at the beginning and during the persistence of the disease, regardless of whether the patient quit smoking, with EETosis debris probably triggering uncontrolled NETosis. The main target of these findings should be young smokers with the potential to develop COPD.Fil: Echevarría, Loli Uribe. Sanatorio Allende; ArgentinaFil: Leimgruber, Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina. Universidad Nacional de Córdoba;Facultad de Ciencias Médicas;Cátedra de Bioquímica Molecular; ArgentinaFil: García González, Jorge. Sanatorio Allende; ArgentinaFil: Nevado, Alberto. Sanatorio Allende; ArgentinaFil: Álvarez, Ruth. Nuevo Hospital San Roque; ArgentinaFil: García, Luciana Noemí. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina. Universidad Nacional de Córdoba;Facultad de Ciencias Médicas;Cátedra de Bioquímica Molecular; ArgentinaFil: Quintar, Amado Alfredo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina. Universidad Nacional de Córdoba;Facultad de Ciencias Médicas;Cátedra de Bioquímica Molecular; ArgentinaFil: Maldonado, Cristina Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina. Universidad Nacional de Córdoba;Facultad de Ciencias Médicas;Cátedra de Bioquímica Molecular; ArgentinaDove Press2017-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/64235Echevarría, Loli Uribe; Leimgruber, Carolina; García González, Jorge; Nevado, Alberto; Álvarez, Ruth; et al.; Evidence of eosinophil extracellular trap cell death in copd: Does it represent the trigger that switches on the disease?; Dove Press; International Journal of COPD; 12; 3-2017; 885-8961178-20051176-9106CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.2147/COPD.S115969info:eu-repo/semantics/altIdentifier/url/https://www.dovepress.com/evidence-of-eosinophil-extracellular-trap-cell-death-in-copd-does-it-r-peer-reviewed-article-COPDinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T13:11:44Zoai:ri.conicet.gov.ar:11336/64235instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-10 13:11:44.524CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Evidence of eosinophil extracellular trap cell death in copd: Does it represent the trigger that switches on the disease?
title Evidence of eosinophil extracellular trap cell death in copd: Does it represent the trigger that switches on the disease?
spellingShingle Evidence of eosinophil extracellular trap cell death in copd: Does it represent the trigger that switches on the disease?
Echevarría, Loli Uribe
COPD
EETOSIS
EOSINOPHILS
INDUCED SPUTUM
NETOSIS
NEUTROPHILS
title_short Evidence of eosinophil extracellular trap cell death in copd: Does it represent the trigger that switches on the disease?
title_full Evidence of eosinophil extracellular trap cell death in copd: Does it represent the trigger that switches on the disease?
title_fullStr Evidence of eosinophil extracellular trap cell death in copd: Does it represent the trigger that switches on the disease?
title_full_unstemmed Evidence of eosinophil extracellular trap cell death in copd: Does it represent the trigger that switches on the disease?
title_sort Evidence of eosinophil extracellular trap cell death in copd: Does it represent the trigger that switches on the disease?
dc.creator.none.fl_str_mv Echevarría, Loli Uribe
Leimgruber, Carolina
García González, Jorge
Nevado, Alberto
Álvarez, Ruth
García, Luciana Noemí
Quintar, Amado Alfredo
Maldonado, Cristina Alicia
author Echevarría, Loli Uribe
author_facet Echevarría, Loli Uribe
Leimgruber, Carolina
García González, Jorge
Nevado, Alberto
Álvarez, Ruth
García, Luciana Noemí
Quintar, Amado Alfredo
Maldonado, Cristina Alicia
author_role author
author2 Leimgruber, Carolina
García González, Jorge
Nevado, Alberto
Álvarez, Ruth
García, Luciana Noemí
Quintar, Amado Alfredo
Maldonado, Cristina Alicia
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv COPD
EETOSIS
EOSINOPHILS
INDUCED SPUTUM
NETOSIS
NEUTROPHILS
topic COPD
EETOSIS
EOSINOPHILS
INDUCED SPUTUM
NETOSIS
NEUTROPHILS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv In spite of the numerous studies on chronic obstructive pulmonary disease (COPD), the cellular and molecular basis of the disease’s development remain unclear. Neutrophils and eosinophils are known to be key players in COPD. Recently, neutrophil extracellular trap cell death (NETosis), a mechanism due to decondensation and extrusion of chromatin to form extracellular traps, has been demonstrated in COPD. However, there is limited knowledge about eosinophil extracellular trap cell death (EETosis) and its role in the pathogenesis of COPD. The aim of this study was to evaluate EETosis in stable COPD. Induced sputum obtained from healthy smokers and low exacerbation risk COPD A or B group patients or high exacerbation risk COPD C or D group patients were included. Samples were examined using electron microscopy and immunofluorescence. Healthy smokers (n=10) and COPD A (n=19) group exhibited neutrophilic or paucigranulocytic phenotypes, with NETosis being absent in these patients. In contrast, COPD B (n=29), with eosinophilic or mixed phenotypes, showed EETosis and incipient NETosis. COPD C (n=18) and COPD D groups (n=13) were differentiated from low exacerbation rate-COPD group by the abundant cellular debris, with COPD C group having an eosinophilic pattern and numerous cells undergoing EETosis. A hallmark of this group was the abundant released membranes that often appeared phagocytosed by neutrophils, which coincidentally exhibited early NETosis changes. The COPD D group included patients with a neutrophilic or mixed pattern, with abundant neutrophil extracellular trap-derived material. This study is the first to demonstrate EETosis at different stages of stable COPD. The results suggest a role for eosinophils in COPD pathophysiology, especially at the beginning and during the persistence of the disease, regardless of whether the patient quit smoking, with EETosis debris probably triggering uncontrolled NETosis. The main target of these findings should be young smokers with the potential to develop COPD.
Fil: Echevarría, Loli Uribe. Sanatorio Allende; Argentina
Fil: Leimgruber, Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina. Universidad Nacional de Córdoba;Facultad de Ciencias Médicas;Cátedra de Bioquímica Molecular; Argentina
Fil: García González, Jorge. Sanatorio Allende; Argentina
Fil: Nevado, Alberto. Sanatorio Allende; Argentina
Fil: Álvarez, Ruth. Nuevo Hospital San Roque; Argentina
Fil: García, Luciana Noemí. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina. Universidad Nacional de Córdoba;Facultad de Ciencias Médicas;Cátedra de Bioquímica Molecular; Argentina
Fil: Quintar, Amado Alfredo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina. Universidad Nacional de Córdoba;Facultad de Ciencias Médicas;Cátedra de Bioquímica Molecular; Argentina
Fil: Maldonado, Cristina Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina. Universidad Nacional de Córdoba;Facultad de Ciencias Médicas;Cátedra de Bioquímica Molecular; Argentina
description In spite of the numerous studies on chronic obstructive pulmonary disease (COPD), the cellular and molecular basis of the disease’s development remain unclear. Neutrophils and eosinophils are known to be key players in COPD. Recently, neutrophil extracellular trap cell death (NETosis), a mechanism due to decondensation and extrusion of chromatin to form extracellular traps, has been demonstrated in COPD. However, there is limited knowledge about eosinophil extracellular trap cell death (EETosis) and its role in the pathogenesis of COPD. The aim of this study was to evaluate EETosis in stable COPD. Induced sputum obtained from healthy smokers and low exacerbation risk COPD A or B group patients or high exacerbation risk COPD C or D group patients were included. Samples were examined using electron microscopy and immunofluorescence. Healthy smokers (n=10) and COPD A (n=19) group exhibited neutrophilic or paucigranulocytic phenotypes, with NETosis being absent in these patients. In contrast, COPD B (n=29), with eosinophilic or mixed phenotypes, showed EETosis and incipient NETosis. COPD C (n=18) and COPD D groups (n=13) were differentiated from low exacerbation rate-COPD group by the abundant cellular debris, with COPD C group having an eosinophilic pattern and numerous cells undergoing EETosis. A hallmark of this group was the abundant released membranes that often appeared phagocytosed by neutrophils, which coincidentally exhibited early NETosis changes. The COPD D group included patients with a neutrophilic or mixed pattern, with abundant neutrophil extracellular trap-derived material. This study is the first to demonstrate EETosis at different stages of stable COPD. The results suggest a role for eosinophils in COPD pathophysiology, especially at the beginning and during the persistence of the disease, regardless of whether the patient quit smoking, with EETosis debris probably triggering uncontrolled NETosis. The main target of these findings should be young smokers with the potential to develop COPD.
publishDate 2017
dc.date.none.fl_str_mv 2017-03
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/64235
Echevarría, Loli Uribe; Leimgruber, Carolina; García González, Jorge; Nevado, Alberto; Álvarez, Ruth; et al.; Evidence of eosinophil extracellular trap cell death in copd: Does it represent the trigger that switches on the disease?; Dove Press; International Journal of COPD; 12; 3-2017; 885-896
1178-2005
1176-9106
CONICET Digital
CONICET
url http://hdl.handle.net/11336/64235
identifier_str_mv Echevarría, Loli Uribe; Leimgruber, Carolina; García González, Jorge; Nevado, Alberto; Álvarez, Ruth; et al.; Evidence of eosinophil extracellular trap cell death in copd: Does it represent the trigger that switches on the disease?; Dove Press; International Journal of COPD; 12; 3-2017; 885-896
1178-2005
1176-9106
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.2147/COPD.S115969
info:eu-repo/semantics/altIdentifier/url/https://www.dovepress.com/evidence-of-eosinophil-extracellular-trap-cell-death-in-copd-does-it-r-peer-reviewed-article-COPD
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Dove Press
publisher.none.fl_str_mv Dove Press
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 12.993085

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