Studies on the contribution of PPAR Gamma to tuberculosis physiopathology

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dc.citation.titleFrontiers in Cellular and Infection Microbiology
dc.citation.volume1-12
dc.citation.volume13
dc.creatorDíaz, Ariana
dc.creatorD’Attilio, Luciano David
dc.creatorPenas, Federico
dc.creatorBongiovanni, Bettina
dc.creatorMassa, Estefania
dc.creatorCevey, Agata
dc.creatorSantucci, Natalia
dc.creatorBottasso, Oscar
dc.creatorGoren, Nora
dc.creatorBay, María Luisa
dc.date.accessioned2024-04-19T16:45:56Z
dc.date.available2024-04-19T16:45:56Z
dc.date.issued2023-04-28
dc.description.abstractIntroduction: Tuberculosis (TB) is a major health problem characterized by an immuno-endocrine imbalance: elevated plasma levels of cortisol and pro- and anti-in fl ammatory mediators, as well as reduced levels of dehydroepiandrosterone. The etiological agent, Mycobacterium tuberculosis (Mtb), is captured by pulmonary macrophages (Mf), whose activation is necessary to cope with the control of Mtb, however, excessive activation of the inflammatory response also leads to tissue damage. Glucocorticoids (GC) are critical elements to counteract the immunoinflammatory reaction, and peroxisome proliferator-activated receptors (PPARs) are also involved in this regard. The primary forms of these receptors are PPARϒ, PPARa, and PPARb/d, the former being the most involved in anti-inflammatory responses. In this work, we seek to gain some insight into the contribution of PPARϒ in immunoendocrine-metabolic interactions by focusing on clinical studies in pulmonary TB patients and in vitro experiments on a Mf cell line. Methods and results: We found that TB patients, at the time of diagnosis, showed increased expression of the PPARϒ transcript in their peripheral blood mononuclear cells, positively associated with circulating cortisol and related to disease severity. Given this background, we investigated the expression of PPARϒ (RT-qPCR) in radiation-killed Mtb-stimulated human Mf. The Mtb stimulation of Mf derived from the human line THP1 significantly increased the expression of PPARϒ, while the activation of this receptor by a specific agonist decreased the expression of pro- and anti-inflammatory cytokines (IL-1β and IL-10). As expected, the addition of GC to stimulated cultures reduced IL-1β production, while cortisol treatment together with the PPARϒ agonist lowered the levels of this proinflammatory cytokine in stimulated cultures. The addition of RU486, a glucocorticoid receptor antagonist, only reversed the inhibition produced by the addition of GC. Conclusion: The current results provide a stimulating background for further analysis of the interconnection between PPARs and steroid hormones in the context of Mtb infection.
dc.description.filFil: Díaz, Ariana. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Inmunología Clínica y Experimental de Rosario (IDICER-CONICET); Argentina.
dc.description.filFil: D’Attilio, Luciano David. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Inmunología Clínica y Experimental de Rosario (IDICER-CONICET); Argentina.
dc.description.filFil: Penas, Federico. Universidad de Buenos Aires. Facultad de Medicina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS-CONICET); Argentina.
dc.description.filFil: Bongiovanni, Bettina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Inmunología Clínica y Experimental de Rosario (IDICER-CONICET); Argentina.
dc.description.filFil: Bongiovanni, Bettina. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas; Argentina.
dc.description.filFil: Massa, Estefania. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Inmunología Clínica y Experimental de Rosario (IDICER-CONICET); Argentina.
dc.description.filFil: Massa, Estefania. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas; Argentina.
dc.description.filFil: Cevey, Agata. Universidad de Buenos Aires. Facultad de Medicina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS-CONICET); Argentina.
dc.description.filFil: Santucci, Natalia. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Inmunología Clínica y Experimental de Rosario (IDICER-CONICET); Argentina.
dc.description.filFil: Bottasso, Oscar. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Inmunología Clínica y Experimental de Rosario (IDICER-CONICET); Argentina.
dc.description.filFil: Goren, Nora. Universidad de Buenos Aires. Facultad de Medicina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS-CONICET); Argentina.
dc.description.sponsorshipScientific and Technological Research (FONCyT): PICT-2018-02375
dc.description.sponsorshipUniversidad Nacional de Rosario. Facultad de Ciencias Médicas
dc.identifier.issn2235-2988
dc.identifier.urihttps://hdl.handle.net/2133/26911
dc.language.isoen
dc.publisherFrontiers Media
dc.relation.publisherversionhttps://www.frontiersin.org/articles/10.3389/fcimb.2023.1067464/full
dc.relation.publisherversionhttps://doi.org/10.3389/fcimb.2023.1067464
dc.rightsopenAccess
dc.rights.holderDíaz, Ariana
dc.rights.holderD’Attilio, Luciano David
dc.rights.holderPenas, Federico
dc.rights.holderBongiovanni, Bettina
dc.rights.holderMassa, Estefania
dc.rights.holderCevey, Agata
dc.rights.holderSantucci, Natalia
dc.rights.holderBottasso, Oscar
dc.rights.holderGoren, Nora
dc.rights.holderBay, María Luisa
dc.rights.holderUniversidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas
dc.rights.textAttribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectTuberculosis
dc.subjectCortisol
dc.subjectDHEA
dc.subjectPPARg
dc.subjectInfectious disease
dc.titleStudies on the contribution of PPAR Gamma to tuberculosis physiopathology
dc.typearticulo
dc.type.collectionarticulo
dc.type.versionpublishedVersion

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