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dc.contributor.author
Giambartolomei, Guillermo Hernan
dc.contributor.author
Delpino, María Victoria
dc.date.available
2020-07-31T20:09:42Z
dc.date.issued
2019-12-20
dc.identifier.citation
Giambartolomei, Guillermo Hernan; Delpino, María Victoria; Immunopathogenesis of Hepatic Brucellosis; Frontiers Research Foundation; Frontiers in Cellular and Infection Microbiology; 9; 423; 20-12-2019; 1-9
dc.identifier.issn
2235-2988
dc.identifier.uri
http://hdl.handle.net/11336/110686
dc.description.abstract
The hepatic immune system can induce rapid and controlled responses to pathogenic microorganisms and tumor cells. Accordingly, most of the microorganisms that reach the liver through the blood are eliminated. However, some of them, including Brucella spp., take advantage of the immunotolerant capacity of the liver to persist in the host. Brucella has a predilection for surviving in the reticuloendothelial system, with the liver being the largest organ of this system in the human body. Therefore, its involvement in brucellosis is practically invariable. In patients with active brucellosis, the liver is commonly affected, and the most frequent clinical manifestation is hepatosplenomegaly. The molecular mechanisms implicated in liver damage have been recently elucidated. It has been demonstrated how Brucella interacts with hepatocytes inducing its death by apoptosis. The inflammatory microenvironment and the direct effect of Brucella on hepatic stellate cells (HSC) induce their activation and turn these cells from its quiescent form to their fibrogenic phenotype. This HSC activation induced by Brucella infection relies on the presence of a functional type IV secretion system and the effector protein BPE005 through a mechanism involved in the activation of the autophagic pathway. Finally, the molecular mechanisms of liver brucellosis observed so far are shedding light on how the interaction of Brucella with liver cells may play an important role in the discovery of new targets to control the infection. In this review, we report the current understanding of the interaction between liver structural cells and immune system cells during Brucella infection.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Frontiers Research Foundation
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by/2.5/ar/
dc.subject
FIBROSIS
dc.subject
HEPATOCITE
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INFLAMACIÓN
dc.subject
LIVER
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STELLATE CELLS (ITO CELLS)
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Inmunología
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Medicina Básica
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Immunopathogenesis of Hepatic Brucellosis
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-04-24T17:43:07Z
dc.journal.volume
9
dc.journal.number
423
dc.journal.pagination
1-9
dc.journal.pais
Suiza
dc.journal.ciudad
Lausana
dc.description.fil
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
dc.description.fil
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
dc.journal.title
Frontiers in Cellular and Infection Microbiology
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fcimb.2019.00423/full
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://doi.org/10.3389/fcimb.2019.00423
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