Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosis

Autores
Bongiovanni, Bettina; Mata Espinosa, Dulce; D'attilio, Luciano David; Leon Contreras, Juan Carlos; Marquez Velasco, Ricardo; Bottasso, Oscar Adelmo; Hernandez Pando, Rogelio; Bay, Maria Luisa
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Tuberculosis (TB) is a major health problem requiring an appropriate cell immune response to be controlled. Macrophages play a central role in the response against Mycobacterium tuberculosis (Mtb). Given our prior studies in which adrenal steroids were found to modify the cellular immune responses from TB patients, it was sensible to analyze the immunomodulatory capability of cortisol and DHEA on macrophages infected with Mtb. The human macrophage-like THP-1 cells were infected with the H37Rv strain of Mtb and treated with Cortisol and DHEA at different doses. We monitored phagocytosis, intracellular-bacterial growth, autophagosoma formation, as well as cytokine gene expression and production. Cultures exposed to cortisol showed a decreased production of IL-1β, TNF-α, with DHEA being unable to modify the pattern of cytokine production or to reverse the cortisol inhibitory effects. Interestingly the intra-macrophagic bacterial burden was found reduced by DHEA treatment. While this effect was not related to a different cytokine pattern, in terms their production or mRNA expression, DHEA treatment did promote autophagy in Mtb-infected macrophages, irrespective of Cortisol presence. In essence, the better control of Mtb load by DHEA-treated macrophages seems to be dependent on an autophagic mechanism. The present results are relevant for two reasons as autophagy is not only important for clearance of mycobacteria but also for the prevention of tissue damage.
Fil: Bongiovanni, Bettina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Rosario. Instituto de Inmunología Clínica y Experimental de Rosario; Argentina. Universidad Nacional de Rosario; Argentina
Fil: Mata Espinosa, Dulce. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; México
Fil: D'attilio, Luciano David. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Rosario. Instituto de Inmunología Clínica y Experimental de Rosario; Argentina. Universidad Nacional de Rosario; Argentina
Fil: Leon Contreras, Juan Carlos. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; México
Fil: Marquez Velasco, Ricardo. Instituto Nacional de Cardiología Ignacio Chavez; México
Fil: Bottasso, Oscar Adelmo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Rosario. Instituto de Inmunología Clínica y Experimental de Rosario; Argentina. Universidad Nacional de Rosario; Argentina
Fil: Hernandez Pando, Rogelio. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; México
Fil: Bay, Maria Luisa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Rosario. Instituto de Inmunología Clínica y Experimental de Rosario; Argentina. Universidad Nacional de Rosario; Argentina
Materia
Macrophages
Mycobacterium Tuberculosis
Dehydroepiandrosterone
Cortisol
Autophagy
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:11336/13522
Acceder
id CONICETDig_ccf9fe6a947da60360c540549d1e41f6
oai_identifier_str oai:ri.conicet.gov.ar:11336/13522
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosisBongiovanni, BettinaMata Espinosa, DulceD'attilio, Luciano DavidLeon Contreras, Juan CarlosMarquez Velasco, RicardoBottasso, Oscar AdelmoHernandez Pando, RogelioBay, Maria LuisaMacrophagesMycobacterium TuberculosisDehydroepiandrosteroneCortisolAutophagyhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Tuberculosis (TB) is a major health problem requiring an appropriate cell immune response to be controlled. Macrophages play a central role in the response against Mycobacterium tuberculosis (Mtb). Given our prior studies in which adrenal steroids were found to modify the cellular immune responses from TB patients, it was sensible to analyze the immunomodulatory capability of cortisol and DHEA on macrophages infected with Mtb. The human macrophage-like THP-1 cells were infected with the H37Rv strain of Mtb and treated with Cortisol and DHEA at different doses. We monitored phagocytosis, intracellular-bacterial growth, autophagosoma formation, as well as cytokine gene expression and production. Cultures exposed to cortisol showed a decreased production of IL-1β, TNF-α, with DHEA being unable to modify the pattern of cytokine production or to reverse the cortisol inhibitory effects. Interestingly the intra-macrophagic bacterial burden was found reduced by DHEA treatment. While this effect was not related to a different cytokine pattern, in terms their production or mRNA expression, DHEA treatment did promote autophagy in Mtb-infected macrophages, irrespective of Cortisol presence. In essence, the better control of Mtb load by DHEA-treated macrophages seems to be dependent on an autophagic mechanism. The present results are relevant for two reasons as autophagy is not only important for clearance of mycobacteria but also for the prevention of tissue damage.Fil: Bongiovanni, Bettina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Rosario. Instituto de Inmunología Clínica y Experimental de Rosario; Argentina. Universidad Nacional de Rosario; ArgentinaFil: Mata Espinosa, Dulce. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; MéxicoFil: D'attilio, Luciano David. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Rosario. Instituto de Inmunología Clínica y Experimental de Rosario; Argentina. Universidad Nacional de Rosario; ArgentinaFil: Leon Contreras, Juan Carlos. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; MéxicoFil: Marquez Velasco, Ricardo. Instituto Nacional de Cardiología Ignacio Chavez; MéxicoFil: Bottasso, Oscar Adelmo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Rosario. Instituto de Inmunología Clínica y Experimental de Rosario; Argentina. Universidad Nacional de Rosario; ArgentinaFil: Hernandez Pando, Rogelio. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; MéxicoFil: Bay, Maria Luisa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Rosario. Instituto de Inmunología Clínica y Experimental de Rosario; Argentina. Universidad Nacional de Rosario; ArgentinaElsevier2015-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/13522Bongiovanni, Bettina; Mata Espinosa, Dulce; D'attilio, Luciano David; Leon Contreras, Juan Carlos; Marquez Velasco, Ricardo; et al.; Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosis; Elsevier; Tuberculosis (edinb); 95; 5; 9-2015; 562-5691472-9792enginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.tube.2015.05.011info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S147297921530010Xinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:29:56Zoai:ri.conicet.gov.ar:11336/13522instacron: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:34982025-10-22 11:29:56.415CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosis
title Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosis
spellingShingle Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosis
Bongiovanni, Bettina
Macrophages
Mycobacterium Tuberculosis
Dehydroepiandrosterone
Cortisol
Autophagy
title_short Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosis
title_full Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosis
title_fullStr Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosis
title_full_unstemmed Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosis
title_sort Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosis
dc.creator.none.fl_str_mv Bongiovanni, Bettina
Mata Espinosa, Dulce
D'attilio, Luciano David
Leon Contreras, Juan Carlos
Marquez Velasco, Ricardo
Bottasso, Oscar Adelmo
Hernandez Pando, Rogelio
Bay, Maria Luisa
author Bongiovanni, Bettina
author_facet Bongiovanni, Bettina
Mata Espinosa, Dulce
D'attilio, Luciano David
Leon Contreras, Juan Carlos
Marquez Velasco, Ricardo
Bottasso, Oscar Adelmo
Hernandez Pando, Rogelio
Bay, Maria Luisa
author_role author
author2 Mata Espinosa, Dulce
D'attilio, Luciano David
Leon Contreras, Juan Carlos
Marquez Velasco, Ricardo
Bottasso, Oscar Adelmo
Hernandez Pando, Rogelio
Bay, Maria Luisa
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Macrophages
Mycobacterium Tuberculosis
Dehydroepiandrosterone
Cortisol
Autophagy
topic Macrophages
Mycobacterium Tuberculosis
Dehydroepiandrosterone
Cortisol
Autophagy
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Tuberculosis (TB) is a major health problem requiring an appropriate cell immune response to be controlled. Macrophages play a central role in the response against Mycobacterium tuberculosis (Mtb). Given our prior studies in which adrenal steroids were found to modify the cellular immune responses from TB patients, it was sensible to analyze the immunomodulatory capability of cortisol and DHEA on macrophages infected with Mtb. The human macrophage-like THP-1 cells were infected with the H37Rv strain of Mtb and treated with Cortisol and DHEA at different doses. We monitored phagocytosis, intracellular-bacterial growth, autophagosoma formation, as well as cytokine gene expression and production. Cultures exposed to cortisol showed a decreased production of IL-1β, TNF-α, with DHEA being unable to modify the pattern of cytokine production or to reverse the cortisol inhibitory effects. Interestingly the intra-macrophagic bacterial burden was found reduced by DHEA treatment. While this effect was not related to a different cytokine pattern, in terms their production or mRNA expression, DHEA treatment did promote autophagy in Mtb-infected macrophages, irrespective of Cortisol presence. In essence, the better control of Mtb load by DHEA-treated macrophages seems to be dependent on an autophagic mechanism. The present results are relevant for two reasons as autophagy is not only important for clearance of mycobacteria but also for the prevention of tissue damage.
Fil: Bongiovanni, Bettina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Rosario. Instituto de Inmunología Clínica y Experimental de Rosario; Argentina. Universidad Nacional de Rosario; Argentina
Fil: Mata Espinosa, Dulce. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; México
Fil: D'attilio, Luciano David. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Rosario. Instituto de Inmunología Clínica y Experimental de Rosario; Argentina. Universidad Nacional de Rosario; Argentina
Fil: Leon Contreras, Juan Carlos. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; México
Fil: Marquez Velasco, Ricardo. Instituto Nacional de Cardiología Ignacio Chavez; México
Fil: Bottasso, Oscar Adelmo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Rosario. Instituto de Inmunología Clínica y Experimental de Rosario; Argentina. Universidad Nacional de Rosario; Argentina
Fil: Hernandez Pando, Rogelio. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; México
Fil: Bay, Maria Luisa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Rosario. Instituto de Inmunología Clínica y Experimental de Rosario; Argentina. Universidad Nacional de Rosario; Argentina
description Tuberculosis (TB) is a major health problem requiring an appropriate cell immune response to be controlled. Macrophages play a central role in the response against Mycobacterium tuberculosis (Mtb). Given our prior studies in which adrenal steroids were found to modify the cellular immune responses from TB patients, it was sensible to analyze the immunomodulatory capability of cortisol and DHEA on macrophages infected with Mtb. The human macrophage-like THP-1 cells were infected with the H37Rv strain of Mtb and treated with Cortisol and DHEA at different doses. We monitored phagocytosis, intracellular-bacterial growth, autophagosoma formation, as well as cytokine gene expression and production. Cultures exposed to cortisol showed a decreased production of IL-1β, TNF-α, with DHEA being unable to modify the pattern of cytokine production or to reverse the cortisol inhibitory effects. Interestingly the intra-macrophagic bacterial burden was found reduced by DHEA treatment. While this effect was not related to a different cytokine pattern, in terms their production or mRNA expression, DHEA treatment did promote autophagy in Mtb-infected macrophages, irrespective of Cortisol presence. In essence, the better control of Mtb load by DHEA-treated macrophages seems to be dependent on an autophagic mechanism. The present results are relevant for two reasons as autophagy is not only important for clearance of mycobacteria but also for the prevention of tissue damage.
publishDate 2015
dc.date.none.fl_str_mv 2015-09
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/11336/13522
Bongiovanni, Bettina; Mata Espinosa, Dulce; D'attilio, Luciano David; Leon Contreras, Juan Carlos; Marquez Velasco, Ricardo; et al.; Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosis; Elsevier; Tuberculosis (edinb); 95; 5; 9-2015; 562-569
1472-9792
url http://hdl.handle.net/11336/13522
identifier_str_mv Bongiovanni, Bettina; Mata Espinosa, Dulce; D'attilio, Luciano David; Leon Contreras, Juan Carlos; Marquez Velasco, Ricardo; et al.; Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosis; Elsevier; Tuberculosis (edinb); 95; 5; 9-2015; 562-569
1472-9792
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.tube.2015.05.011
info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S147297921530010X
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
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
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 12.982451

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