Evaluation of glucocorticoid sensitivity in peripheral blood mononuclear cell from patients with Tuberculosis

GALLUCCI, GEORGINA; ESTEFANÍA, MASSA; IMHOFF, MATILDE; DIAB, MAGDALENA; DIAZ, ARIANA ; BONGIOVANNI, BETTINA; SANTUCCI, NATALIA; DERIO, MARISA; BERTOLA, DIEGO; DI MASSO. RICARDO; BOTTASSO, OSCAR; BAY, MARÍA LUISA; DATTILIO, LUCIANO

Mar del Plata . Buenos Aires

Congreso; REUNIÓN CONJUNTA SAIC SAI&FAIC SAFIS 2022; 2022

Sociedad Argentina de Inmunología

Tuberculosis (TB), is a major worldwide health problem, caused by Mycobacterium tuberculosis (Mtb). Previous studies in patients with pulmonary TB showed an immuno-endocrine imbalance characterized by a disease-severity associated increase in plasma levels of proinflammatory cytokines and glucocorticoids (GCs). Moreover, a decreased ratio of glucocorticoid receptor transcript isoform (GRα/GRβ), unfavourable to cortisol action, was detected. This may be in line with certain degree of GC endogenous resistance, mainly in cases with progressive disease. In chronic diseases as TB, cortisol plays a crucial role modulating immune response and diminishing tissue damage. To date, it has never been assessed a functional assay of GC sensitivity in TB patients. Hence, GCs sensitivity in peripheral blood mononuclear cell (PBMCs) from TB patients (n=8) and Healthy controls (HCo) (n=8) stimulated with Mtb irradiated (Mtbi) in the presence of different doses Cortisol (5.10-5-10-8M) was evaluated. The GC effect was measured by quantifying Mtbi-induced-Interleukin-6 (IL-6, ELISA) inhibition in 24h cultures supernatant. Doses-response curves from different groups were analysed as two-way repeated measures analysis of variance (ANOVA). As expected, cortisol produced a significant dose-dependent inhibition of IL-6 production [F= 11.4; p