DHEA modulates the oxidative species production in THP1-derived macrophages exposed to irradiated Mycobacterium tuberculosis

BETTINA BONGIOVANNI; ARÍSTIDES POCHETTINO; RAPHAELLE DRÉAN; ROCÍO DEL VALLE FERNÁNDEZ; OSCAR BOTTASSO; MARÍA L. BAY

Buenos Aires

Congreso; LXIII Annual Meeting of the Argentinean Society for Immunology, IV Meeting of LASID and II French-Argentinean Immunology Congress; 2015

Sociedad Argentina de Inmunología

Tuberculosis is an ancient disease caused by the intracellular pathogen Mycobacterium tuberculosis (Mtb). Macrophages play a central role in the response against Mtb. Our previous work demonstrated that the response of macrophages infected with Mtb was modulated by cortisol (Gc) and dehydroepiandrosterone (DHEA). In fact, DHEA at physiological conditions (that is in presence of Gc) increased phagocytosis, autophagy induction, while decreasing the number of colony-forming unity (CFU). Expanding this issue we have now studied some intracellular processes, i.e., oxidant species, which may be involved in these phenomena. Macrophages derived from THP-1 cell line were exposed to Mtb gamma irradiated (Mtbi) during 3 or 24 h in presence or absence of Gc (1 μM) and/or DHEA (1 and 0.1μM), n=5 for treatment). Upon washing, cells were used to evaluate the oxidative status including reactive oxygen species (ROS) generation, L-Glutathione reduced (GSH) levels and antioxidant enzyme activities. The results showed that ROS and catalase activity increased with DHEA in presence of Gc treatments at 24 h respect to Mtbi alone and control cultures (p