M1 macrophage polarization is dependent on TRPC1-mediated calcium entry

Abstract: 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) γ priming of naive macrophages induces store-mediated Ca2+ entry and inhibition of Ca2+ entry impairs pol...

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Autores principales: 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.
Formato: Artículo
Lenguaje:Inglés
Publicado: Elsevier (Cell Press) 2019
Materias:
INMUNOLOGIA
SISTEMA INMUNOLOGICO
CALCIO
SEPSIS
Acceso en línea:https://repositorio.uca.edu.ar/handle/123456789/8685
Aporte de:
Repositorio Institucional de la Universidad Católica Argentina (UCA) de Universidad Católica Argentina
id I33-R139123456789-8685
record_format dspace
institution Universidad Católica Argentina
institution_str I-33
repository_str R-139
collection Repositorio Institucional de la Universidad Católica Argentina (UCA)
language Inglés
topic INMUNOLOGIA
SISTEMA INMUNOLOGICO
CALCIO
SEPSIS
spellingShingle INMUNOLOGIA
SISTEMA INMUNOLOGICO
CALCIO
SEPSIS
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.
M1 macrophage polarization is dependent on TRPC1-mediated calcium entry
topic_facet INMUNOLOGIA
SISTEMA INMUNOLOGICO
CALCIO
SEPSIS
description Abstract: 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) γ 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 IFNγ-induced Ca2+ influx was mediated by TRPC1. Deficiency of TRPC1 displayed abrogated IFNγ-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.
format Artículo
author 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_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_sort Chauhan, Arun
title M1 macrophage polarization is dependent on TRPC1-mediated calcium entry
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
publisher Elsevier (Cell Press)
publishDate 2019
url https://repositorio.uca.edu.ar/handle/123456789/8685
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