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

BONGIOVANNI BETTINA; POCHETTINO ARISTIDES; DRÉAN RAPHAELLE; FERNANDEZ ROCIO DEL VALLE; BOTTASSO OSCAR; BAY MARÍA LUISA

BuenosAires

Congreso; Congress of Latin American Society for Immunodeficiencies (LASID 2015), Sociedad Argentina de Inmunología (SAI) y Sociedad Francesa de Inmunología (SFI); 2015

Latin American Society for Immunodeficiencies (LASID 2015), Sociedad Argentina de Inmunología (SAI) y Sociedad Francesa de Inmunología (SFI)

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