Brucella abortus Infection Promotes Mesenchymal Stem Cell Differentiation Toward Adipogenesis, Enhancing the Proinflammatory Profile

Autores
Freiberger, Rosa Nicole; López, Cynthia Alicia Marcela; Palma, Maria Belen; Cevallos, Cintia Gisela; Sviercz, Franco Agustin; Jarmoluk, Patricio Gabriel; García, Marcela Nilda; Quarleri, Jorge Fabian; Delpino, María Victoria
Año de publicación
2026
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The most common complication of active brucellosis in humans is osteoarticular injury. Inthe bone marrow microenvironment, mesenchymal stem cells (MSCs) can differentiate intoeither adipocytes or osteoblasts, and this balance is tightly regulated because an increase inadipogenesis may negatively affect bone formation and favor bone loss. The differentiationof MSCs into adipocytes or osteoblasts is tightly regulated by mechanisms that promote cellfate toward one lineage while repressing the other. Our study demonstrated that Brucellaabortus infects MSCs but does not affect the deposition of organic and mineral matrixduring osteoblast differentiation. However, the infection upregulates Receptor Activator ofNuclear Factor Kappa-B Ligand (RANKL) expression in osteoblasts, which may contributeto osteoclast activation and bone resorption. Conversely, B. abortus infection significantlyinfluences adipocyte differentiation by modulating lipolysis, lipogenesis, and interactionsbetween lipid droplets and mitochondria. This leads to increased cellular cholesterol levelsand reduced intracellular triglycerides, accompanied by glycerol release. These changes result in more differentiated adipocytes and larger lipid droplets. Consequently, we observedincreased IL-6 secretion and a higher leptin/adiponectin ratio. Importantly, these effectswere independent of a functional type IV secretion system (T4SS), as purified Brucella DNAfully reproduced the adipogenic phenotype. Moreover, inhibition of TLR9—the primarysensor of bacterial DNA—significantly reduced the DNA-induced adipogenic response,demonstrating that adipocyte modulation is at least in part mediated through TLR9 signaling. In summary, B. abortus promotes MSC differentiation toward an inflammatoryadipocyte phenotype. It involves a TLR-9-mediated DNA detection. It may contribute toosteoarticular injury and infection-associated bone resorption.
Fil: Freiberger, Rosa Nicole. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: López, Cynthia Alicia Marcela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Palma, Maria Belen. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias. Departamento de Ciencias Básicas. Cátedra de Histología y Embriología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Cevallos, Cintia Gisela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Sviercz, Franco Agustin. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Jarmoluk, Patricio Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: García, Marcela Nilda. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias. Departamento de Ciencias Básicas. Cátedra de Histología y Embriología; Argentina
Fil: Quarleri, Jorge Fabian. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Delpino, María Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Materia
brucellosis
MSCs
osteoblasts
osteoarticular
adipocyte
leptin
lipid-droplets
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/288703
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/288703
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network_name_str CONICET Digital (CONICET)
spelling Brucella abortus Infection Promotes Mesenchymal Stem Cell Differentiation Toward Adipogenesis, Enhancing the Proinflammatory ProfileFreiberger, Rosa NicoleLópez, Cynthia Alicia MarcelaPalma, Maria BelenCevallos, Cintia GiselaSviercz, Franco AgustinJarmoluk, Patricio GabrielGarcía, Marcela NildaQuarleri, Jorge FabianDelpino, María VictoriabrucellosisMSCsosteoblastsosteoarticularadipocyteleptinlipid-dropletshttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3The most common complication of active brucellosis in humans is osteoarticular injury. Inthe bone marrow microenvironment, mesenchymal stem cells (MSCs) can differentiate intoeither adipocytes or osteoblasts, and this balance is tightly regulated because an increase inadipogenesis may negatively affect bone formation and favor bone loss. The differentiationof MSCs into adipocytes or osteoblasts is tightly regulated by mechanisms that promote cellfate toward one lineage while repressing the other. Our study demonstrated that Brucellaabortus infects MSCs but does not affect the deposition of organic and mineral matrixduring osteoblast differentiation. However, the infection upregulates Receptor Activator ofNuclear Factor Kappa-B Ligand (RANKL) expression in osteoblasts, which may contributeto osteoclast activation and bone resorption. Conversely, B. abortus infection significantlyinfluences adipocyte differentiation by modulating lipolysis, lipogenesis, and interactionsbetween lipid droplets and mitochondria. This leads to increased cellular cholesterol levelsand reduced intracellular triglycerides, accompanied by glycerol release. These changes result in more differentiated adipocytes and larger lipid droplets. Consequently, we observedincreased IL-6 secretion and a higher leptin/adiponectin ratio. Importantly, these effectswere independent of a functional type IV secretion system (T4SS), as purified Brucella DNAfully reproduced the adipogenic phenotype. Moreover, inhibition of TLR9—the primarysensor of bacterial DNA—significantly reduced the DNA-induced adipogenic response,demonstrating that adipocyte modulation is at least in part mediated through TLR9 signaling. In summary, B. abortus promotes MSC differentiation toward an inflammatoryadipocyte phenotype. It involves a TLR-9-mediated DNA detection. It may contribute toosteoarticular injury and infection-associated bone resorption.Fil: Freiberger, Rosa Nicole. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: López, Cynthia Alicia Marcela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Palma, Maria Belen. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias. Departamento de Ciencias Básicas. Cátedra de Histología y Embriología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Cevallos, Cintia Gisela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Sviercz, Franco Agustin. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Jarmoluk, Patricio Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: García, Marcela Nilda. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias. Departamento de Ciencias Básicas. Cátedra de Histología y Embriología; ArgentinaFil: Quarleri, Jorge Fabian. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Delpino, María Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaMDPI2026-04info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/288703Freiberger, Rosa Nicole; López, Cynthia Alicia Marcela; Palma, Maria Belen; Cevallos, Cintia Gisela; Sviercz, Franco Agustin; et al.; Brucella abortus Infection Promotes Mesenchymal Stem Cell Differentiation Toward Adipogenesis, Enhancing the Proinflammatory Profile; MDPI; Tropical Medicine and Infectious Disease; 11; 5; 4-2026; 1-202414-6366CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/2414-6366/11/5/112info:eu-repo/semantics/altIdentifier/doi/10.3390/tropicalmed11050112info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2026-08-25T14:33:46Zoai:ri.conicet.gov.ar:11336/288703instacron: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:34982026-08-25 14:33:47.148CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Brucella abortus Infection Promotes Mesenchymal Stem Cell Differentiation Toward Adipogenesis, Enhancing the Proinflammatory Profile
title Brucella abortus Infection Promotes Mesenchymal Stem Cell Differentiation Toward Adipogenesis, Enhancing the Proinflammatory Profile
spellingShingle Brucella abortus Infection Promotes Mesenchymal Stem Cell Differentiation Toward Adipogenesis, Enhancing the Proinflammatory Profile
Freiberger, Rosa Nicole
brucellosis
MSCs
osteoblasts
osteoarticular
adipocyte
leptin
lipid-droplets
title_short Brucella abortus Infection Promotes Mesenchymal Stem Cell Differentiation Toward Adipogenesis, Enhancing the Proinflammatory Profile
title_full Brucella abortus Infection Promotes Mesenchymal Stem Cell Differentiation Toward Adipogenesis, Enhancing the Proinflammatory Profile
title_fullStr Brucella abortus Infection Promotes Mesenchymal Stem Cell Differentiation Toward Adipogenesis, Enhancing the Proinflammatory Profile
title_full_unstemmed Brucella abortus Infection Promotes Mesenchymal Stem Cell Differentiation Toward Adipogenesis, Enhancing the Proinflammatory Profile
title_sort Brucella abortus Infection Promotes Mesenchymal Stem Cell Differentiation Toward Adipogenesis, Enhancing the Proinflammatory Profile
dc.creator.none.fl_str_mv Freiberger, Rosa Nicole
López, Cynthia Alicia Marcela
Palma, Maria Belen
Cevallos, Cintia Gisela
Sviercz, Franco Agustin
Jarmoluk, Patricio Gabriel
García, Marcela Nilda
Quarleri, Jorge Fabian
Delpino, María Victoria
author Freiberger, Rosa Nicole
author_facet Freiberger, Rosa Nicole
López, Cynthia Alicia Marcela
Palma, Maria Belen
Cevallos, Cintia Gisela
Sviercz, Franco Agustin
Jarmoluk, Patricio Gabriel
García, Marcela Nilda
Quarleri, Jorge Fabian
Delpino, María Victoria
author_role author
author2 López, Cynthia Alicia Marcela
Palma, Maria Belen
Cevallos, Cintia Gisela
Sviercz, Franco Agustin
Jarmoluk, Patricio Gabriel
García, Marcela Nilda
Quarleri, Jorge Fabian
Delpino, María Victoria
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv brucellosis
MSCs
osteoblasts
osteoarticular
adipocyte
leptin
lipid-droplets
topic brucellosis
MSCs
osteoblasts
osteoarticular
adipocyte
leptin
lipid-droplets
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The most common complication of active brucellosis in humans is osteoarticular injury. Inthe bone marrow microenvironment, mesenchymal stem cells (MSCs) can differentiate intoeither adipocytes or osteoblasts, and this balance is tightly regulated because an increase inadipogenesis may negatively affect bone formation and favor bone loss. The differentiationof MSCs into adipocytes or osteoblasts is tightly regulated by mechanisms that promote cellfate toward one lineage while repressing the other. Our study demonstrated that Brucellaabortus infects MSCs but does not affect the deposition of organic and mineral matrixduring osteoblast differentiation. However, the infection upregulates Receptor Activator ofNuclear Factor Kappa-B Ligand (RANKL) expression in osteoblasts, which may contributeto osteoclast activation and bone resorption. Conversely, B. abortus infection significantlyinfluences adipocyte differentiation by modulating lipolysis, lipogenesis, and interactionsbetween lipid droplets and mitochondria. This leads to increased cellular cholesterol levelsand reduced intracellular triglycerides, accompanied by glycerol release. These changes result in more differentiated adipocytes and larger lipid droplets. Consequently, we observedincreased IL-6 secretion and a higher leptin/adiponectin ratio. Importantly, these effectswere independent of a functional type IV secretion system (T4SS), as purified Brucella DNAfully reproduced the adipogenic phenotype. Moreover, inhibition of TLR9—the primarysensor of bacterial DNA—significantly reduced the DNA-induced adipogenic response,demonstrating that adipocyte modulation is at least in part mediated through TLR9 signaling. In summary, B. abortus promotes MSC differentiation toward an inflammatoryadipocyte phenotype. It involves a TLR-9-mediated DNA detection. It may contribute toosteoarticular injury and infection-associated bone resorption.
Fil: Freiberger, Rosa Nicole. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: López, Cynthia Alicia Marcela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Palma, Maria Belen. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias. Departamento de Ciencias Básicas. Cátedra de Histología y Embriología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Cevallos, Cintia Gisela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Sviercz, Franco Agustin. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Jarmoluk, Patricio Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: García, Marcela Nilda. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias. Departamento de Ciencias Básicas. Cátedra de Histología y Embriología; Argentina
Fil: Quarleri, Jorge Fabian. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Delpino, María Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
description The most common complication of active brucellosis in humans is osteoarticular injury. Inthe bone marrow microenvironment, mesenchymal stem cells (MSCs) can differentiate intoeither adipocytes or osteoblasts, and this balance is tightly regulated because an increase inadipogenesis may negatively affect bone formation and favor bone loss. The differentiationof MSCs into adipocytes or osteoblasts is tightly regulated by mechanisms that promote cellfate toward one lineage while repressing the other. Our study demonstrated that Brucellaabortus infects MSCs but does not affect the deposition of organic and mineral matrixduring osteoblast differentiation. However, the infection upregulates Receptor Activator ofNuclear Factor Kappa-B Ligand (RANKL) expression in osteoblasts, which may contributeto osteoclast activation and bone resorption. Conversely, B. abortus infection significantlyinfluences adipocyte differentiation by modulating lipolysis, lipogenesis, and interactionsbetween lipid droplets and mitochondria. This leads to increased cellular cholesterol levelsand reduced intracellular triglycerides, accompanied by glycerol release. These changes result in more differentiated adipocytes and larger lipid droplets. Consequently, we observedincreased IL-6 secretion and a higher leptin/adiponectin ratio. Importantly, these effectswere independent of a functional type IV secretion system (T4SS), as purified Brucella DNAfully reproduced the adipogenic phenotype. Moreover, inhibition of TLR9—the primarysensor of bacterial DNA—significantly reduced the DNA-induced adipogenic response,demonstrating that adipocyte modulation is at least in part mediated through TLR9 signaling. In summary, B. abortus promotes MSC differentiation toward an inflammatoryadipocyte phenotype. It involves a TLR-9-mediated DNA detection. It may contribute toosteoarticular injury and infection-associated bone resorption.
publishDate 2026
dc.date.none.fl_str_mv 2026-04
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/11336/288703
Freiberger, Rosa Nicole; López, Cynthia Alicia Marcela; Palma, Maria Belen; Cevallos, Cintia Gisela; Sviercz, Franco Agustin; et al.; Brucella abortus Infection Promotes Mesenchymal Stem Cell Differentiation Toward Adipogenesis, Enhancing the Proinflammatory Profile; MDPI; Tropical Medicine and Infectious Disease; 11; 5; 4-2026; 1-20
2414-6366
CONICET Digital
CONICET
url http://hdl.handle.net/11336/288703
identifier_str_mv Freiberger, Rosa Nicole; López, Cynthia Alicia Marcela; Palma, Maria Belen; Cevallos, Cintia Gisela; Sviercz, Franco Agustin; et al.; Brucella abortus Infection Promotes Mesenchymal Stem Cell Differentiation Toward Adipogenesis, Enhancing the Proinflammatory Profile; MDPI; Tropical Medicine and Infectious Disease; 11; 5; 4-2026; 1-20
2414-6366
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/2414-6366/11/5/112
info:eu-repo/semantics/altIdentifier/doi/10.3390/tropicalmed11050112
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 MDPI
publisher.none.fl_str_mv MDPI
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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