Transcript expression for immune and endocrine mediators in THP1-derived macrophages infected with Mycobacterium tuberculosis exposed to cortisol and/or DHEA

BONGIOVANNI B; D´ATTILIO L; MATA D; MARQUINA CASTILLO B; BOTTASSO O; HERNANDEZ PANDO R; BAY ML

Mar del Plata

Congreso; LIX Reunión Científica Anual de la SAIC, Mar del Plata 19-22 Noviembre de 2014; 2014

Sociedad Argentina de Investigación Clínica

Macrophages play a central role in the response against Mycobacterium tuberculosis (Mtb). Our previous work demonstrated that the response of macrophages infected to Mtb was modulated by cortisol (Gc) and dehydroepiandrosterone (DHEA). In fact, combined treatment with both steroids increased Mtb phagocytosis but decreased the number of colony-forming units; for which we decided to analyze the possible intracellular mechanisms involved in this process. Macrophages derived from the THP-1 cell line were exposed to live Mtb strain H37Rv (MOI 5:1) during 3 hr in presence or absence of Gc (1 uM) and/or DHEA (1 and 0.1μM). Upon washing, cells were cultured for 24 hr in the same media with or without hormones to further analyze several cell transcripts by qRT-PCR. That is the expression of glucocorticoid receptors, alpha y beta (GRalpha and GRbeta), enzyme regulating cortisol availability (11-beta-hydroxysteroid dehydrogenase type 1 -11BHSD1- and type 2 -11BHSD2-) and pro-apoptotic proteins (Caspases), the inflammasome related protein (NLRP) and inducible nitric oxide synthase (iNOS). Results showed that Gc inhibited GRa, 11BHSD1 and caspase 1 expression (p