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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/13522
Ver los metadatos del registro completo
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oai:ri.conicet.gov.ar:11336/13522 |
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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 Técnicas2025-09-29T10:00:25Zoai: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:34982025-09-29 10:00:25.815CONICET 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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1844613785691619328 |
score |
13.070432 |