M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry

Autores
Chauhan, Arun; Sun, Yuyang; Sukumaran, Pramod; Quenum Zangbede, Fredice O.; Jondle, Christopher N.; Sharma, Atul; Evans, Dustin L.; Chauhan, Pooja; Szlabick, Randolph E.; Aaland, Mary O.; Birnbaumer, Lutz; Sharma, Jyotika; Singh, Brij B.; Mishra, Bibhuti B.
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Macrophage plasticity is essential for innate immunity, but in-depth signaling mechanism(s) regulating their functional phenotypes are ill-defined. Here we report that interferon (IFN) g priming of naive macrophages induces store-mediated Ca2+ entry and inhibition of Ca2+ entry impairs polarization to M1 inflammatory phenotype. In vitro and in vivo functional analyses revealed ORAI1 to be a primary contributor to basal Ca2+ influx in macrophages, whereas IFNg-induced Ca2+ influx was mediated by TRPC1. Deficiency of TRPC1 displayed abrogated IFNg-induced M1 inflammatory mediators in macrophages. In a preclinical model of peritonitis by Klebsiella pneumoniae infection, macrophages showed increased Ca2+ influx, which was TRPC1 dependent. Macrophages from infected TRPC1 / mice showed inhibited expression of M1-associated signature molecules. Furthermore, in human patients with systemic inflammatory response syndrome, the level of TRPC1 expression in circulating macrophages directly correlated with M1 inflammatory mediators. Overall, TRPC1-mediated Ca2+ influx is essential for the induction/shaping of macrophage polarization to M1 inflammatory phenotype.
Fil: Chauhan, Arun. University of North Dakota; Estados Unidos
Fil: Sun, Yuyang. Texas A&M University; Estados Unidos. University of North Dakota; Estados Unidos
Fil: Sukumaran, Pramod. Texas A&M University; Estados Unidos. University of North Dakota; Estados Unidos
Fil: Quenum Zangbede, Fredice O.. University of North Dakota; Estados Unidos
Fil: Jondle, Christopher N.. University of North Dakota; Estados Unidos
Fil: Sharma, Atul. University of North Dakota; Estados Unidos
Fil: Evans, Dustin L.. University of North Dakota; Estados Unidos
Fil: Chauhan, Pooja. University of North Dakota; Estados Unidos
Fil: Szlabick, Randolph E.. University of North Dakota; Estados Unidos
Fil: Aaland, Mary O.. University of North Dakota; Estados Unidos
Fil: Birnbaumer, Lutz. 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. National Institutes of Health; Estados Unidos
Fil: Sharma, Jyotika. University of North Dakota; Estados Unidos
Fil: Singh, Brij B.. University of North Dakota; Estados Unidos
Fil: Mishra, Bibhuti B.. University of North Dakota; Estados Unidos
Materia
BIOLOGICAL SCIENCES
IMMUNE RESPONSE
IMMUNOLOGY
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/99403
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/99403
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium EntryChauhan, ArunSun, YuyangSukumaran, PramodQuenum Zangbede, Fredice O.Jondle, Christopher N.Sharma, AtulEvans, Dustin L.Chauhan, PoojaSzlabick, Randolph E.Aaland, Mary O.Birnbaumer, LutzSharma, JyotikaSingh, Brij B.Mishra, Bibhuti B.BIOLOGICAL SCIENCESIMMUNE RESPONSEIMMUNOLOGYhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Macrophage plasticity is essential for innate immunity, but in-depth signaling mechanism(s) regulating their functional phenotypes are ill-defined. Here we report that interferon (IFN) g priming of naive macrophages induces store-mediated Ca2+ entry and inhibition of Ca2+ entry impairs polarization to M1 inflammatory phenotype. In vitro and in vivo functional analyses revealed ORAI1 to be a primary contributor to basal Ca2+ influx in macrophages, whereas IFNg-induced Ca2+ influx was mediated by TRPC1. Deficiency of TRPC1 displayed abrogated IFNg-induced M1 inflammatory mediators in macrophages. In a preclinical model of peritonitis by Klebsiella pneumoniae infection, macrophages showed increased Ca2+ influx, which was TRPC1 dependent. Macrophages from infected TRPC1 / mice showed inhibited expression of M1-associated signature molecules. Furthermore, in human patients with systemic inflammatory response syndrome, the level of TRPC1 expression in circulating macrophages directly correlated with M1 inflammatory mediators. Overall, TRPC1-mediated Ca2+ influx is essential for the induction/shaping of macrophage polarization to M1 inflammatory phenotype.Fil: Chauhan, Arun. University of North Dakota; Estados UnidosFil: Sun, Yuyang. Texas A&M University; Estados Unidos. University of North Dakota; Estados UnidosFil: Sukumaran, Pramod. Texas A&M University; Estados Unidos. University of North Dakota; Estados UnidosFil: Quenum Zangbede, Fredice O.. University of North Dakota; Estados UnidosFil: Jondle, Christopher N.. University of North Dakota; Estados UnidosFil: Sharma, Atul. University of North Dakota; Estados UnidosFil: Evans, Dustin L.. University of North Dakota; Estados UnidosFil: Chauhan, Pooja. University of North Dakota; Estados UnidosFil: Szlabick, Randolph E.. University of North Dakota; Estados UnidosFil: Aaland, Mary O.. University of North Dakota; Estados UnidosFil: Birnbaumer, Lutz. 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. National Institutes of Health; Estados UnidosFil: Sharma, Jyotika. University of North Dakota; Estados UnidosFil: Singh, Brij B.. University of North Dakota; Estados UnidosFil: Mishra, Bibhuti B.. University of North Dakota; Estados UnidosElsevier Inc.2018-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/99403Chauhan, Arun; Sun, Yuyang; Sukumaran, Pramod; Quenum Zangbede, Fredice O.; Jondle, Christopher N.; et al.; M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry; Elsevier Inc.; iScience; 8; 10-2018; 85-1022589-0042CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.isci.2018.09.014info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S2589004218301494info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:13:34Zoai:ri.conicet.gov.ar:11336/99403instacron: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 15:13:34.48CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry
title M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry
spellingShingle M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry
Chauhan, Arun
BIOLOGICAL SCIENCES
IMMUNE RESPONSE
IMMUNOLOGY
title_short M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry
title_full M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry
title_fullStr M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry
title_full_unstemmed M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry
title_sort M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry
dc.creator.none.fl_str_mv Chauhan, Arun
Sun, Yuyang
Sukumaran, Pramod
Quenum Zangbede, Fredice O.
Jondle, Christopher N.
Sharma, Atul
Evans, Dustin L.
Chauhan, Pooja
Szlabick, Randolph E.
Aaland, Mary O.
Birnbaumer, Lutz
Sharma, Jyotika
Singh, Brij B.
Mishra, Bibhuti B.
author Chauhan, Arun
author_facet Chauhan, Arun
Sun, Yuyang
Sukumaran, Pramod
Quenum Zangbede, Fredice O.
Jondle, Christopher N.
Sharma, Atul
Evans, Dustin L.
Chauhan, Pooja
Szlabick, Randolph E.
Aaland, Mary O.
Birnbaumer, Lutz
Sharma, Jyotika
Singh, Brij B.
Mishra, Bibhuti B.
author_role author
author2 Sun, Yuyang
Sukumaran, Pramod
Quenum Zangbede, Fredice O.
Jondle, Christopher N.
Sharma, Atul
Evans, Dustin L.
Chauhan, Pooja
Szlabick, Randolph E.
Aaland, Mary O.
Birnbaumer, Lutz
Sharma, Jyotika
Singh, Brij B.
Mishra, Bibhuti B.
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv BIOLOGICAL SCIENCES
IMMUNE RESPONSE
IMMUNOLOGY
topic BIOLOGICAL SCIENCES
IMMUNE RESPONSE
IMMUNOLOGY
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Macrophage plasticity is essential for innate immunity, but in-depth signaling mechanism(s) regulating their functional phenotypes are ill-defined. Here we report that interferon (IFN) g priming of naive macrophages induces store-mediated Ca2+ entry and inhibition of Ca2+ entry impairs polarization to M1 inflammatory phenotype. In vitro and in vivo functional analyses revealed ORAI1 to be a primary contributor to basal Ca2+ influx in macrophages, whereas IFNg-induced Ca2+ influx was mediated by TRPC1. Deficiency of TRPC1 displayed abrogated IFNg-induced M1 inflammatory mediators in macrophages. In a preclinical model of peritonitis by Klebsiella pneumoniae infection, macrophages showed increased Ca2+ influx, which was TRPC1 dependent. Macrophages from infected TRPC1 / mice showed inhibited expression of M1-associated signature molecules. Furthermore, in human patients with systemic inflammatory response syndrome, the level of TRPC1 expression in circulating macrophages directly correlated with M1 inflammatory mediators. Overall, TRPC1-mediated Ca2+ influx is essential for the induction/shaping of macrophage polarization to M1 inflammatory phenotype.
Fil: Chauhan, Arun. University of North Dakota; Estados Unidos
Fil: Sun, Yuyang. Texas A&M University; Estados Unidos. University of North Dakota; Estados Unidos
Fil: Sukumaran, Pramod. Texas A&M University; Estados Unidos. University of North Dakota; Estados Unidos
Fil: Quenum Zangbede, Fredice O.. University of North Dakota; Estados Unidos
Fil: Jondle, Christopher N.. University of North Dakota; Estados Unidos
Fil: Sharma, Atul. University of North Dakota; Estados Unidos
Fil: Evans, Dustin L.. University of North Dakota; Estados Unidos
Fil: Chauhan, Pooja. University of North Dakota; Estados Unidos
Fil: Szlabick, Randolph E.. University of North Dakota; Estados Unidos
Fil: Aaland, Mary O.. University of North Dakota; Estados Unidos
Fil: Birnbaumer, Lutz. 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. National Institutes of Health; Estados Unidos
Fil: Sharma, Jyotika. University of North Dakota; Estados Unidos
Fil: Singh, Brij B.. University of North Dakota; Estados Unidos
Fil: Mishra, Bibhuti B.. University of North Dakota; Estados Unidos
description Macrophage plasticity is essential for innate immunity, but in-depth signaling mechanism(s) regulating their functional phenotypes are ill-defined. Here we report that interferon (IFN) g priming of naive macrophages induces store-mediated Ca2+ entry and inhibition of Ca2+ entry impairs polarization to M1 inflammatory phenotype. In vitro and in vivo functional analyses revealed ORAI1 to be a primary contributor to basal Ca2+ influx in macrophages, whereas IFNg-induced Ca2+ influx was mediated by TRPC1. Deficiency of TRPC1 displayed abrogated IFNg-induced M1 inflammatory mediators in macrophages. In a preclinical model of peritonitis by Klebsiella pneumoniae infection, macrophages showed increased Ca2+ influx, which was TRPC1 dependent. Macrophages from infected TRPC1 / mice showed inhibited expression of M1-associated signature molecules. Furthermore, in human patients with systemic inflammatory response syndrome, the level of TRPC1 expression in circulating macrophages directly correlated with M1 inflammatory mediators. Overall, TRPC1-mediated Ca2+ influx is essential for the induction/shaping of macrophage polarization to M1 inflammatory phenotype.
publishDate 2018
dc.date.none.fl_str_mv 2018-10
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/11336/99403
Chauhan, Arun; Sun, Yuyang; Sukumaran, Pramod; Quenum Zangbede, Fredice O.; Jondle, Christopher N.; et al.; M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry; Elsevier Inc.; iScience; 8; 10-2018; 85-102
2589-0042
CONICET Digital
CONICET
url http://hdl.handle.net/11336/99403
identifier_str_mv Chauhan, Arun; Sun, Yuyang; Sukumaran, Pramod; Quenum Zangbede, Fredice O.; Jondle, Christopher N.; et al.; M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry; Elsevier Inc.; iScience; 8; 10-2018; 85-102
2589-0042
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.isci.2018.09.014
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S2589004218301494
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Inc.
publisher.none.fl_str_mv Elsevier 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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score 13.22299

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