Adrenal Steroids Modulate Fibroblast-Like Synoviocytes Response During B. abortus Infection
- Autores
- Gentilini, Maria Virginia; Giambartolomei, Guillermo Hernan; Delpino, María Victoria
- Año de publicación
- 2019
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Brucella abortus stimulates an inflammatory immune response that stimulates theendocrine system, inducing the secretion of dehydroepiandrosterone (DHEA) andcortisol. In humans, the active disease is generally present as osteoarticular brucellosis.In previous studies we showed that B. abortus infection of synoviocytes creates aproinflammatory microenvironment. We proposed to determine the role of cortisoland DHEA on synoviocytes and infiltrating monocytes during B. abortus infection.Cortisol inhibited IL-6, IL-8, MCP-1, and MMP-2 secretion induced by B. abortusinfection in synovial fibroblast. Cortisol-mediated MMP-2 inhibition during B. abortusinfection was reversed by IL-6. DHEA inhibited B. abortus-induced RANKL up-regulationin synovial fibroblast through estrogen receptor (ER). B. abortus infection did notmodulate glucocorticoid receptor (GR) expression. Cell responses to cortisol alsodepended on its intracellular bioavailability, according to the activity of the isoenzymes11b-hydroxysteroid dehydrogenase (HSD) type-1 and 11b-HSD2 (which are involvedin cortisone-cortisol interconversion). B. abortus infection did not modify 11b-HSD1expression and GRa/b ratio in the presence or absence of adrenal steroids. Supernatantsfrom B. abortus-infected monocytes induced 11b-HSD1 in synovial cells. Administrationof cortisone was capable of inhibiting the secretion of RANKL by synoviocytes mimickingcortisol?s effect. These results go along with previous observations that highlighted theability of synovial tissue to secrete active steroids, making it an intracrine tissue. This isthe first study that contributes to the knowledge of the consequence of adrenal steroidson synoviocytes in the context of a bacterial infection.
Fil: Gentilini, Maria Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Fil: Giambartolomei, Guillermo Hernan. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Fil: Delpino, María Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina - Materia
- BRUCELLA
- Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/110667
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Adrenal Steroids Modulate Fibroblast-Like Synoviocytes Response During B. abortus InfectionGentilini, Maria VirginiaGiambartolomei, Guillermo HernanDelpino, María VictoriaBRUCELLAhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Brucella abortus stimulates an inflammatory immune response that stimulates theendocrine system, inducing the secretion of dehydroepiandrosterone (DHEA) andcortisol. In humans, the active disease is generally present as osteoarticular brucellosis.In previous studies we showed that B. abortus infection of synoviocytes creates aproinflammatory microenvironment. We proposed to determine the role of cortisoland DHEA on synoviocytes and infiltrating monocytes during B. abortus infection.Cortisol inhibited IL-6, IL-8, MCP-1, and MMP-2 secretion induced by B. abortusinfection in synovial fibroblast. Cortisol-mediated MMP-2 inhibition during B. abortusinfection was reversed by IL-6. DHEA inhibited B. abortus-induced RANKL up-regulationin synovial fibroblast through estrogen receptor (ER). B. abortus infection did notmodulate glucocorticoid receptor (GR) expression. Cell responses to cortisol alsodepended on its intracellular bioavailability, according to the activity of the isoenzymes11b-hydroxysteroid dehydrogenase (HSD) type-1 and 11b-HSD2 (which are involvedin cortisone-cortisol interconversion). B. abortus infection did not modify 11b-HSD1expression and GRa/b ratio in the presence or absence of adrenal steroids. Supernatantsfrom B. abortus-infected monocytes induced 11b-HSD1 in synovial cells. Administrationof cortisone was capable of inhibiting the secretion of RANKL by synoviocytes mimickingcortisol?s effect. These results go along with previous observations that highlighted theability of synovial tissue to secrete active steroids, making it an intracrine tissue. This isthe first study that contributes to the knowledge of the consequence of adrenal steroidson synoviocytes in the context of a bacterial infection.Fil: Gentilini, Maria Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFil: Giambartolomei, Guillermo Hernan. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFil: Delpino, María Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFrontiers Research Foundation2019-10-22info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/110667Gentilini, Maria Virginia; Giambartolomei, Guillermo Hernan; Delpino, María Victoria; Adrenal Steroids Modulate Fibroblast-Like Synoviocytes Response During B. abortus Infection; Frontiers Research Foundation; Frontiers in Endocrinology; 10; 22-10-2019; 1-12; 7221664-2392CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.3389/fendo.2019.00722info:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fendo.2019.00722/fullinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:40:56Zoai:ri.conicet.gov.ar:11336/110667instacron: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 09:40:56.982CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Adrenal Steroids Modulate Fibroblast-Like Synoviocytes Response During B. abortus Infection |
title |
Adrenal Steroids Modulate Fibroblast-Like Synoviocytes Response During B. abortus Infection |
spellingShingle |
Adrenal Steroids Modulate Fibroblast-Like Synoviocytes Response During B. abortus Infection Gentilini, Maria Virginia BRUCELLA |
title_short |
Adrenal Steroids Modulate Fibroblast-Like Synoviocytes Response During B. abortus Infection |
title_full |
Adrenal Steroids Modulate Fibroblast-Like Synoviocytes Response During B. abortus Infection |
title_fullStr |
Adrenal Steroids Modulate Fibroblast-Like Synoviocytes Response During B. abortus Infection |
title_full_unstemmed |
Adrenal Steroids Modulate Fibroblast-Like Synoviocytes Response During B. abortus Infection |
title_sort |
Adrenal Steroids Modulate Fibroblast-Like Synoviocytes Response During B. abortus Infection |
dc.creator.none.fl_str_mv |
Gentilini, Maria Virginia Giambartolomei, Guillermo Hernan Delpino, María Victoria |
author |
Gentilini, Maria Virginia |
author_facet |
Gentilini, Maria Virginia Giambartolomei, Guillermo Hernan Delpino, María Victoria |
author_role |
author |
author2 |
Giambartolomei, Guillermo Hernan Delpino, María Victoria |
author2_role |
author author |
dc.subject.none.fl_str_mv |
BRUCELLA |
topic |
BRUCELLA |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Brucella abortus stimulates an inflammatory immune response that stimulates theendocrine system, inducing the secretion of dehydroepiandrosterone (DHEA) andcortisol. In humans, the active disease is generally present as osteoarticular brucellosis.In previous studies we showed that B. abortus infection of synoviocytes creates aproinflammatory microenvironment. We proposed to determine the role of cortisoland DHEA on synoviocytes and infiltrating monocytes during B. abortus infection.Cortisol inhibited IL-6, IL-8, MCP-1, and MMP-2 secretion induced by B. abortusinfection in synovial fibroblast. Cortisol-mediated MMP-2 inhibition during B. abortusinfection was reversed by IL-6. DHEA inhibited B. abortus-induced RANKL up-regulationin synovial fibroblast through estrogen receptor (ER). B. abortus infection did notmodulate glucocorticoid receptor (GR) expression. Cell responses to cortisol alsodepended on its intracellular bioavailability, according to the activity of the isoenzymes11b-hydroxysteroid dehydrogenase (HSD) type-1 and 11b-HSD2 (which are involvedin cortisone-cortisol interconversion). B. abortus infection did not modify 11b-HSD1expression and GRa/b ratio in the presence or absence of adrenal steroids. Supernatantsfrom B. abortus-infected monocytes induced 11b-HSD1 in synovial cells. Administrationof cortisone was capable of inhibiting the secretion of RANKL by synoviocytes mimickingcortisol?s effect. These results go along with previous observations that highlighted theability of synovial tissue to secrete active steroids, making it an intracrine tissue. This isthe first study that contributes to the knowledge of the consequence of adrenal steroidson synoviocytes in the context of a bacterial infection. Fil: Gentilini, Maria Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Giambartolomei, Guillermo Hernan. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Delpino, María Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina |
description |
Brucella abortus stimulates an inflammatory immune response that stimulates theendocrine system, inducing the secretion of dehydroepiandrosterone (DHEA) andcortisol. In humans, the active disease is generally present as osteoarticular brucellosis.In previous studies we showed that B. abortus infection of synoviocytes creates aproinflammatory microenvironment. We proposed to determine the role of cortisoland DHEA on synoviocytes and infiltrating monocytes during B. abortus infection.Cortisol inhibited IL-6, IL-8, MCP-1, and MMP-2 secretion induced by B. abortusinfection in synovial fibroblast. Cortisol-mediated MMP-2 inhibition during B. abortusinfection was reversed by IL-6. DHEA inhibited B. abortus-induced RANKL up-regulationin synovial fibroblast through estrogen receptor (ER). B. abortus infection did notmodulate glucocorticoid receptor (GR) expression. Cell responses to cortisol alsodepended on its intracellular bioavailability, according to the activity of the isoenzymes11b-hydroxysteroid dehydrogenase (HSD) type-1 and 11b-HSD2 (which are involvedin cortisone-cortisol interconversion). B. abortus infection did not modify 11b-HSD1expression and GRa/b ratio in the presence or absence of adrenal steroids. Supernatantsfrom B. abortus-infected monocytes induced 11b-HSD1 in synovial cells. Administrationof cortisone was capable of inhibiting the secretion of RANKL by synoviocytes mimickingcortisol?s effect. These results go along with previous observations that highlighted theability of synovial tissue to secrete active steroids, making it an intracrine tissue. This isthe first study that contributes to the knowledge of the consequence of adrenal steroidson synoviocytes in the context of a bacterial infection. |
publishDate |
2019 |
dc.date.none.fl_str_mv |
2019-10-22 |
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/11336/110667 Gentilini, Maria Virginia; Giambartolomei, Guillermo Hernan; Delpino, María Victoria; Adrenal Steroids Modulate Fibroblast-Like Synoviocytes Response During B. abortus Infection; Frontiers Research Foundation; Frontiers in Endocrinology; 10; 22-10-2019; 1-12; 722 1664-2392 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/110667 |
identifier_str_mv |
Gentilini, Maria Virginia; Giambartolomei, Guillermo Hernan; Delpino, María Victoria; Adrenal Steroids Modulate Fibroblast-Like Synoviocytes Response During B. abortus Infection; Frontiers Research Foundation; Frontiers in Endocrinology; 10; 22-10-2019; 1-12; 722 1664-2392 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.3389/fendo.2019.00722 info:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fendo.2019.00722/full |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Frontiers Research Foundation |
publisher.none.fl_str_mv |
Frontiers Research Foundation |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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