Expression of ANX1, GILZ, FKBP5, NFKBIA and NFKBIB genes and its association with alpha and beta isoforms of glucocorticoid receptor in patients with Tuberculosis.

DÍAZ, ARIANA; SANTUCCI NATALIA; D'ATTILIO, LUCIANO; GALLUCCI, GEORGINA; FERNÁNDEZ, ROCÍO DEL VALLE; BÉRTOLA, DIEGO; BAY, MARÍA LUISA; IMHOFF, MATILDE; BONGIOVANNI, BETTINA; BOTTASSO, OSCAR A.

Congreso; SLAMTB 2020; 2020

Sociedad Latinoamericana de micobacterias y Tuberculosis

Tuberculosis is the leading cause of death worldwide attributed to an infection agent, M. Tuberculosis. As a chronic disease, pulmonary tuberculosis (TB) exhibits a protracted inflammation along with several immunoendocrine-metabolic alterations. Regarding the hypothalamic-pituitary-adrenal axis (HPA), newly diagnosed TB patients (TBps) show high levels of plasma cortisol as well as pro- and anti-inflammatory mediators while dehydroepiandosterone (DHEA) levels are found quite low and associated with disease severity. In turn, severe TBps show a certain degree of resistance to the anti-inflammatory action of endogenous cortisol, as mRNA levels from the glucocorticoid receptor negative isoform (GRβ) are increased, without changes in levels of the bioactive isoform (GRα).Extending these findings, we now quantified (RT-qPCR) GR-related genes (ANXA1, GILZ, FKBP5, NFKBIA and NFKBIB) in PBMC from adult TBps (n=47) and healthy controls (HCo, n=47). mRNA levels from AnxA1, GILZ, NFKBIA and NFKBIB were significantly increased in TBps (p