IL-1 beta;, PGE2 AND IFNalpha; REGULATE THE AUTOPHAGY PROCESS IN MONOCYTES FROM TUBERCULOSIS PATIENTS

CANDELA MARTIN , ; MARÍA PAULA MORELLI ; NANCY L.TATEOSIAN ; NICOLAS OSCAR AMIANO ; LUCIA DONNOLI ; CAMILA MARTINENA ; LORENA CIALLELLA ; ROSA MUSELLA ; GRACIELA CASADO ; DOMINGO PALMERO ; VERÓNICA EDITH GARCÍA

Congreso; Reunión conjunta SAIC-SAI-AAFE-NANOMED.AR 2022; 2022

INTRODUCTION: Autophagy plays a crucial role in immunity against intracellular pathogens. We previously reported that both IFN- 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 healthy donors (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