Expression of GAL-1, GAL-3 and GAL-9 in macrophages infected with Mtb and its modulation by cortisol and dehidroepiandrosterone

D'ATTILIO LUCIANO; BONGIOVANNI BETTINA; FERNANDEZ ROCIO DEL VALLE; DIAZ ARIANA; CERLIANI JUAN PABLO; HERNANDEZ PANDO ROGELIO; RABINOVICH GABRIEL; BOTTASSO OSCAR; BAY MARÍA LUISA

Mar del Plata

Congreso; LXVI Congreso de la Sociedad Argentina de Inmunología; 2018

Tuberculosis (TB) is an ancient disease caused by the intracellular pathogen Mycobacterium tuberculosis (Mtb). We previously demonstrated that patients with pulmonary TB have increased plasma levels of pro and anti-inflammatory cytokines, cortisol, Galectin-1 (Gal) and Gal-3, along with a marked decrease in dehydroepiandrosterone (DHEA). Macrophage function which play a central role in the response against Mtb, were also found modulated by cortisol (Gc) and DHEA. At physiological conditions, DHEA (in presence of Gc) increased phagocytosis, autophagy induction, while decreasing the number of colony-forming units. Expanding this issue and given the central immunomodulatory role of galectins, we now studied the expression of mRNA for Gal-1, Gal-3 and Gal-9 in cultured macrophages (derived from THP-1 cell line (Mf -THP-1) infected with Mtb in presence or absence of Gc (1 μM) and/or DHEA (0.1 μM), during 24 h (n = 5/treatment). Mtb-infection increased the expression of Gal-3 in Mf-THP-1 respect to uninfected cultures, with Gal-1 and Gal-9 showing no differences. Treatments with hormones separately did not modify the Mtb-induced effect. However, the combination of both hormones increased and decreased significantly the expression of Gal-9 and Gal-1, respectively, respect to only stimulated cultures; implying an important role in bacterial clearance.