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dc.creatorAltamirano Silva, Pamela
dc.creatorCordero Serrano, Marlen
dc.creatorMéndez Montoya, Joselyn
dc.creatorChacón Díaz, Carlos
dc.creatorGuzmán Verri, Caterina
dc.creatorMoreno Robles, Edgardo
dc.creatorChaves Olarte, Esteban
dc.date.accessioned2021-04-29T20:26:06Z
dc.date.available2021-04-29T20:26:06Z
dc.date.issued2021
dc.identifier.issn1098-5522
dc.identifier.urihttps://hdl.handle.net/10669/83327
dc.description.abstractBrucella abortus is a facultative extracellular-intracellular pathogen that encounters a diversity of environments within the host cell. We report that bacteria extracted from infected cells at late stages (48 h post-infection) of the intracellular life cycle significantly increase their ability to multiply in new target cells. This increase depends on early interaction with the cell surface since bacteria become more adherent and penetrate more efficiently as compared to in vitro grown bacteria. At this late stage of infection, the bacterium locates within an autophagosome-like compartment, facing starving and acidic conditions. At this point, the two-component system BvrR/BvrS becomes activated, and the expression of the transcriptional regulator VjbR and the type IV secretion system VirB increased. Using bafilomycin to inhibit BvrR/BvrS activation and specific inhibitors for VjbR and VirB we showed that the BvrR/BvrS and VjbR systems correlate with the increased interaction with new host cells while the VirB system does not. Bacteria released from infected cells under natural conditions displayed the same phenotype as intracellular bacteria. We propose a model in which the B. abortus BvrR/BvrS system senses the transition from its replicative niche at the endoplasmic reticulum to the autophagosome-like exit compartment. This activation leads to the expression of VirB participating in the release of the bacterium from the cells and an increase in VjbR expression that results in a more efficient interaction with new host cells.es_ES
dc.language.isoenges_ES
dc.sourceInfection and Immunityes_ES
dc.subjectbrucellosises_ES
dc.subjectintracellular life cyclees_ES
dc.subjectvirulence circuites_ES
dc.titleIntracellular passage triggers a molecular response in that increases its infectiousnesses_ES
dc.typeartículo científico
dc.date.updated2021-04-26T21:12:12Z
dc.identifier.doi10.1128/IAI.00004-21
dc.description.procedenceUCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias de la Salud::Centro de Investigación en Enfermedades Tropicales (CIET)es_ES


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