IL-1 β, PGE2 AND IFNα REGULATE THE AUTOPHAGY PROCESS IN MONOCYTES FROM TUBERCULOSIS PATIENTS

CANDELA MARTIN; MARÍA PAULA MORELLI; NANCY TATEOSIAN; NICOLÁS O. AMIANO; LUCIA DONNOLLI; CAMILA MARTINENA; LORENA CIALLELLA; ROSA MARÍA MUSELLA; GRACIELA M. GRAGNOLINI DE CASADO; PALMERO DOMINGO; VERÓNICA E. GARCIA

Mar del Plata

Congreso; Reunión Conjunta SAIC ? SAI ? SAFIS; 2022

Introduction: Autophagy plays a crucial role in immunity against intracellular pathogens. We previously reported that both IFN-g and IL-17A influenced autophagy during human tuberculosis (TB). Both IL-1 and IFNα/β represent two main cross regulated inflammatory cytokines during Mycobacterium tuberculosis (Mtb) infection. Moreover, IL-1 and IFNα/β are functionally connected via eicosanoids like PGE2. Here we studied the potential role of these immune mediators on the autophagy of Mtb in monocytes from TB patients.Methods: Tuberculosis (TB) patients were classified as low and high responders (LR and HR, respectively) according to their immune responses to sonicated Mtb (Mtb-Ag). Control individuals were healthydonors (HD) from the community. Monocytes were obtained from heparinized peripheral blood and cultured (2x10’6cs/ml) with an Mtb lysate (Mtb-Ag, 10μg/ml) ± IL-1β (10ng/ml), IFNα (10ng/ml) o PGE2 (2nM). Flow cytometry was used to evaluate autophagy levels. P-values