Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured Cells

Autores
Clauzure, Mariangeles; Valdivieso, Ángel Gabriel; Massip Copiz, María Macarena; Mori, Consuelo; Dugour, Andrea Vanesa; Figueroa, Juan Manuel; Santa Coloma, Tomás Antonio
Año de publicación
2017
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Cystic fibrosis (CF) is caused by mutations in the CFTR gene, which encodes a cAMP‐regulated chloride channel. Several cellular functions are altered in CF cells. However, it is not clear how the CFTR failure induces those alterations. We have found previously several genes differentially expressed in CF cells, including c‐Src, MUC1, MTND4, and CISD1 (CFTR‐dependent genes). Recently, we also reported the existence of several chloride‐dependent genes, among them GLRX5 and RPS27. Here, varying the intracellular chloride concentration [Cl−]i of IB3‐1 CF bronchial epithelial cells, we show that IL‐1β mRNA expression and secretion are also under Cl− modulation. The response to Cl− is biphasic, with maximal effects at 75 mM Cl−. The regulation of the IL‐1β mRNA expression involves an IL‐1β autocrine effect, since in the presence of the IL‐1β receptor antagonist IL1RN or anti‐IL‐1β blocking antibody, the mRNA response to Cl− disappeared. Similar effects were obtained with the JNK inhibitor SP600125, the c‐Src inhibitor PP2 and the IKK inhibitor III (BMS‐345541). On the other hand, the IL‐1β secretion is still modulated by Cl− in the presence of IL‐1RN, IL‐1β blocking antibody, or cycloheximide, suggesting that Cl− is affecting the IL‐1β maturation/secretion, which in turn starts an autocrine positive feedback loop. In conclusion, the Cl− anion acts as a second messenger for CFTR, modulating the IL‐1β maturation/secretion. The results also imply that, depending on its intracellular concentration, Cl− could be a pro‐inflammatory mediator.
Fil: Clauzure, Mariangeles. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Mori, Consuelo. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Dugour, Andrea Vanesa. Fundación Pablo Cassara; Argentina
Fil: Figueroa, Juan Manuel. Fundación Pablo Cassara; Argentina
Fil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Materia
CFTR
Cystic fibrosis
IL-1b
Chloride
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:11336/47642
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/47642
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured CellsClauzure, MariangelesValdivieso, Ángel GabrielMassip Copiz, María MacarenaMori, ConsueloDugour, Andrea VanesaFigueroa, Juan ManuelSanta Coloma, Tomás AntonioCFTRCystic fibrosisIL-1bChloridehttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Cystic fibrosis (CF) is caused by mutations in the CFTR gene, which encodes a cAMP‐regulated chloride channel. Several cellular functions are altered in CF cells. However, it is not clear how the CFTR failure induces those alterations. We have found previously several genes differentially expressed in CF cells, including c‐Src, MUC1, MTND4, and CISD1 (CFTR‐dependent genes). Recently, we also reported the existence of several chloride‐dependent genes, among them GLRX5 and RPS27. Here, varying the intracellular chloride concentration [Cl−]i of IB3‐1 CF bronchial epithelial cells, we show that IL‐1β mRNA expression and secretion are also under Cl− modulation. The response to Cl− is biphasic, with maximal effects at 75 mM Cl−. The regulation of the IL‐1β mRNA expression involves an IL‐1β autocrine effect, since in the presence of the IL‐1β receptor antagonist IL1RN or anti‐IL‐1β blocking antibody, the mRNA response to Cl− disappeared. Similar effects were obtained with the JNK inhibitor SP600125, the c‐Src inhibitor PP2 and the IKK inhibitor III (BMS‐345541). On the other hand, the IL‐1β secretion is still modulated by Cl− in the presence of IL‐1RN, IL‐1β blocking antibody, or cycloheximide, suggesting that Cl− is affecting the IL‐1β maturation/secretion, which in turn starts an autocrine positive feedback loop. In conclusion, the Cl− anion acts as a second messenger for CFTR, modulating the IL‐1β maturation/secretion. The results also imply that, depending on its intracellular concentration, Cl− could be a pro‐inflammatory mediator.Fil: Clauzure, Mariangeles. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaFil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaFil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaFil: Mori, Consuelo. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaFil: Dugour, Andrea Vanesa. Fundación Pablo Cassara; ArgentinaFil: Figueroa, Juan Manuel. Fundación Pablo Cassara; ArgentinaFil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaWiley-liss, Div John Wiley & Sons Inc2017-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/47642Clauzure, Mariangeles; Valdivieso, Ángel Gabriel; Massip Copiz, María Macarena; Mori, Consuelo; Dugour, Andrea Vanesa; et al.; Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured Cells; Wiley-liss, Div John Wiley & Sons Inc; Journal of Cellular Biochemistry; 118; 8; 8-2017; 2131-21400730-2312CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1002/jcb.25850info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1002/jcb.25850info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T14:38:14Zoai:ri.conicet.gov.ar:11336/47642instacron: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:34982025-10-15 14:38:14.916CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured Cells
title Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured Cells
spellingShingle Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured Cells
Clauzure, Mariangeles
CFTR
Cystic fibrosis
IL-1b
Chloride
title_short Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured Cells
title_full Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured Cells
title_fullStr Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured Cells
title_full_unstemmed Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured Cells
title_sort Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured Cells
dc.creator.none.fl_str_mv Clauzure, Mariangeles
Valdivieso, Ángel Gabriel
Massip Copiz, María Macarena
Mori, Consuelo
Dugour, Andrea Vanesa
Figueroa, Juan Manuel
Santa Coloma, Tomás Antonio
author Clauzure, Mariangeles
author_facet Clauzure, Mariangeles
Valdivieso, Ángel Gabriel
Massip Copiz, María Macarena
Mori, Consuelo
Dugour, Andrea Vanesa
Figueroa, Juan Manuel
Santa Coloma, Tomás Antonio
author_role author
author2 Valdivieso, Ángel Gabriel
Massip Copiz, María Macarena
Mori, Consuelo
Dugour, Andrea Vanesa
Figueroa, Juan Manuel
Santa Coloma, Tomás Antonio
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv CFTR
Cystic fibrosis
IL-1b
Chloride
topic CFTR
Cystic fibrosis
IL-1b
Chloride
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Cystic fibrosis (CF) is caused by mutations in the CFTR gene, which encodes a cAMP‐regulated chloride channel. Several cellular functions are altered in CF cells. However, it is not clear how the CFTR failure induces those alterations. We have found previously several genes differentially expressed in CF cells, including c‐Src, MUC1, MTND4, and CISD1 (CFTR‐dependent genes). Recently, we also reported the existence of several chloride‐dependent genes, among them GLRX5 and RPS27. Here, varying the intracellular chloride concentration [Cl−]i of IB3‐1 CF bronchial epithelial cells, we show that IL‐1β mRNA expression and secretion are also under Cl− modulation. The response to Cl− is biphasic, with maximal effects at 75 mM Cl−. The regulation of the IL‐1β mRNA expression involves an IL‐1β autocrine effect, since in the presence of the IL‐1β receptor antagonist IL1RN or anti‐IL‐1β blocking antibody, the mRNA response to Cl− disappeared. Similar effects were obtained with the JNK inhibitor SP600125, the c‐Src inhibitor PP2 and the IKK inhibitor III (BMS‐345541). On the other hand, the IL‐1β secretion is still modulated by Cl− in the presence of IL‐1RN, IL‐1β blocking antibody, or cycloheximide, suggesting that Cl− is affecting the IL‐1β maturation/secretion, which in turn starts an autocrine positive feedback loop. In conclusion, the Cl− anion acts as a second messenger for CFTR, modulating the IL‐1β maturation/secretion. The results also imply that, depending on its intracellular concentration, Cl− could be a pro‐inflammatory mediator.
Fil: Clauzure, Mariangeles. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Mori, Consuelo. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Dugour, Andrea Vanesa. Fundación Pablo Cassara; Argentina
Fil: Figueroa, Juan Manuel. Fundación Pablo Cassara; Argentina
Fil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
description Cystic fibrosis (CF) is caused by mutations in the CFTR gene, which encodes a cAMP‐regulated chloride channel. Several cellular functions are altered in CF cells. However, it is not clear how the CFTR failure induces those alterations. We have found previously several genes differentially expressed in CF cells, including c‐Src, MUC1, MTND4, and CISD1 (CFTR‐dependent genes). Recently, we also reported the existence of several chloride‐dependent genes, among them GLRX5 and RPS27. Here, varying the intracellular chloride concentration [Cl−]i of IB3‐1 CF bronchial epithelial cells, we show that IL‐1β mRNA expression and secretion are also under Cl− modulation. The response to Cl− is biphasic, with maximal effects at 75 mM Cl−. The regulation of the IL‐1β mRNA expression involves an IL‐1β autocrine effect, since in the presence of the IL‐1β receptor antagonist IL1RN or anti‐IL‐1β blocking antibody, the mRNA response to Cl− disappeared. Similar effects were obtained with the JNK inhibitor SP600125, the c‐Src inhibitor PP2 and the IKK inhibitor III (BMS‐345541). On the other hand, the IL‐1β secretion is still modulated by Cl− in the presence of IL‐1RN, IL‐1β blocking antibody, or cycloheximide, suggesting that Cl− is affecting the IL‐1β maturation/secretion, which in turn starts an autocrine positive feedback loop. In conclusion, the Cl− anion acts as a second messenger for CFTR, modulating the IL‐1β maturation/secretion. The results also imply that, depending on its intracellular concentration, Cl− could be a pro‐inflammatory mediator.
publishDate 2017
dc.date.none.fl_str_mv 2017-08
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/11336/47642
Clauzure, Mariangeles; Valdivieso, Ángel Gabriel; Massip Copiz, María Macarena; Mori, Consuelo; Dugour, Andrea Vanesa; et al.; Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured Cells; Wiley-liss, Div John Wiley & Sons Inc; Journal of Cellular Biochemistry; 118; 8; 8-2017; 2131-2140
0730-2312
CONICET Digital
CONICET
url http://hdl.handle.net/11336/47642
identifier_str_mv Clauzure, Mariangeles; Valdivieso, Ángel Gabriel; Massip Copiz, María Macarena; Mori, Consuelo; Dugour, Andrea Vanesa; et al.; Intracellular Chloride Concentration Changes Modulate IL-1β Expression and Secretion in Human Bronchial Epithelial Cultured Cells; Wiley-liss, Div John Wiley & Sons Inc; Journal of Cellular Biochemistry; 118; 8; 8-2017; 2131-2140
0730-2312
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1002/jcb.25850
info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1002/jcb.25850
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
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Wiley-liss, Div John Wiley & Sons Inc
publisher.none.fl_str_mv Wiley-liss, Div John Wiley & Sons Inc
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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