Examinando por Autor "Villar, Silvina Raquel"

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    Death of adrenocortical cells during murine acute T. cruzi infection is not associated with TNF-R1 signaling but mostly with the type II pathway of Fas-mediated apoptosis
    (Academic Press Inc Elsevier Science, 2017-10) Pérez, Ana Rosa; Lambertucci, Flavia; González, Florencia Belén; Roggero, Eduardo Angel; Bottasso, Oscar; de Meis, Juliana; Ronco, Maria Teresa; Villar, Silvina Raquel
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    Dysregulated Network of Immune, Endocrine and Metabolic Markers is Associated to More Severe Human Chronic Chagas Cardiomyopathy
    (S. Karger AG, 2018-09-25) González, Florencia Belén; Villar, Silvina Raquel; D'Attilio, Luciano; Leiva, Rodolfo; Marquez, Julia; Lioi, Susana; Beloscar, Juan; Bottasso, Oscar; Pérez, Ana Rosa
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    Genetic engineering of Lactococcus lactis co-producing antigen and the mucosal adjuvant 3′ 5′- cyclic di adenosine monophosphate (c-di-AMP) as a design strategy to develop a mucosal vaccine prototype
    (Frontiers Media, 2018-09-04) Quintana, Ingrid M.; Espariz, Martín; Villar, Silvina Raquel; González, Florencia Belén; Pacini, María F.; Cabrera, Gabriel; Bontempi, Iván; Prochetto, Estefanía; Stülke, Jörg; Pérez, Ana R. ; Marcipar, Iván; Blancato, Víctor Sebastián; Magni, Christian
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    Tumor Necrosis Factor-α Regulates Glucocorticoid Synthesis in the Adrenal Glands of Trypanosoma cruzi Acutely-Infected Mice. The Role of TNF-R1
    (PLOS (Public Library of Science), 2013-05-22) Villar, Silvina Raquel; Ronco, María Teresa; Fernández Bussy, Rodrigo; Roggero, Eduardo; Lepletier, Ailin; Manarin, Romina; Savino, Wilson; Pérez, Ana Rosa; Bottasso, Oscar
    Adrenal steroidogenesis is under a complex regulation involving extrinsic and intrinsic adrenal factors. TNF-α is an inflammatory cytokine produced in response to tissue injury and several other stimuli. We have previously demonstrated that TNF-R1 knockout (TNF-R1−/−) mice have a dysregulated synthesis of glucocorticoids (GCs) during Trypanosoma cruzi acute infection. Since TNF-α may influence GCs production, not only through the hypothalamus-pituitary axis, but also at the adrenal level, we now investigated the role of this cytokine on the adrenal GCs production. Wild type (WT) and TNF-R1−/− mice undergoing acute infection (Tc-WT and Tc-TNF-R1−/− groups), displayed adrenal hyperplasia together with increased GCs levels. Notably, systemic ACTH remained unchanged in Tc-WT and Tc-TNF-R1−/− compared with uninfected mice, suggesting some degree of ACTH-independence of GCs synthesis. TNF-α expression was increased within the adrenal gland from both infected mouse groups, with Tc-WT mice showing an augmented TNF-R1 expression. Tc-WT mice showed increased levels of P-p38 and P-ERK compared to uninfected WT animals, whereas Tc-TNF-R1−/− mice had increased p38 and JNK phosphorylation respect to Tc-WT mice. Strikingly, adrenal NF-κB and AP-1 activation during infection was blunted in Tc-TNF-R1−/− mice. The accumulation of mRNAs for steroidogenic acute regulatory protein and cytochrome P450 were significantly increased in both Tc-WT and Tc-TNF-R1−/− mice; being much more augmented in the latter group, which also had remarkably increased GCs levels. TNF-α emerges as a potent modulator of steroidogenesis in adrenocortical cells during T. cruzi infection in which MAPK pathways, NF-κB and AP-1 seem to play a role in the adrenal synthesis of pro-inflammatory cytokines and enzymes regulating GCs synthesis. These results suggest the existence of an intrinsic immune-adrenal interaction involved in the dysregulated synthesis of GCs during murine Chagas disease.