STUDY OF GENES REGULATED BY THE GLUCOCORTICOID RECEPTOR IN PERIPHERAL BLOOD AND PLEURAL FLUID MONONUCLEAR CELLS FROM PATIENTS WITH PLEURAL TUBERCULOSIS

GALLUCCI GEORGINA; ESTEFANÍA MASSA 1 ,; MATILDE IMHOFF 1 , ; BETTINA BONGIOVANNI 1 ,; , ARIANA DÍAZ 1 , ; NATALIA SANTUCCI 1 , ; DIEGO BÉRTOLA 2 , ; LIOI SUSANA 2 ,; , MARISA DERIO 1; MARÍA LUISA BAY 1; , OSCAR BOTTASSO 1; LUCIANO D? ATTILIO

Congreso; Reunión Conjunta SAIC . SAI. AAFE. NANOMED. AR; 2021

One of the commonest extrapulmonary manifestations of tuberculosis (TB) is pleuralTB (PLTB). Since the cellular immune response (IR) is essential for the containment andresolution of the infectious process, PLTB constitutes a model to study the protectiveIR at the site of infection, and the ensuing endocrine response. In previous studies, wehave shown that patients with PLTB have a greater inflammatory and cellular responseat the pleural compartment (increase in IL-1β, IL-6 and IFN-ɣ concentrations) respectto the systemic level. Furthermore, mononuclear cells (MC) from pleural exudates(PEMC) had an in vitro high specific proliferative capacity compared to peripheralcounterparts (PBMC), with cortisol levels being only increased at the peripheralcompartment. To expand this issue, PBMC and PEMC from PLTB patients (n=12) wereanalyzed for the expression levels of genes (RT-qPCR) that are positively (ANXA1, GILZ,FKBP5, NFKBIA and NFKBIB) or negatively (IL-1β, IL-6, IFN-ɣ) regulated byglucocorticoid receptor (GR), in addition to the NFkB subunit 1 gene (NFkB1) and theeventual relationship with the circulating immuno-endocrine profile. While showing anincrease in the expression levels of ANXA1, GILZ, NFKBIA in PBMC with respect toPEMC (p