METFORMIN TREATMENT IN MACROPHAGES COULD HAVE AN EFFECT ON T CELL ACTIVATION AGAINST T. CRUZI INFECTION.

BAIGORRÍ, RE; HELLRIEGEL, MF; BRUGO, MB; VAZQUEZ VIGNALE, M; FONTANARI, C; VIANO, ME; RODRIGUEZ GALAN, MC; MOTRAN, CC; STEMPIN, CC; CERBAN, FM

San Luis

Congreso; LXXI Reunión Científica Anual de la Sociedad Argentina de Inmunología.; 2023

Sociedad Argentina de Inmunología.

Macrophages (Mo) play a key role in initial control of T. cruzi replication mainlythrough iNOS expression and ROS production. However, exacerbated ROS andiNOS production could lead to T cell suppression and tissue damage. This canbe modulated by various intracellular signals. AMPK is a cellular energy sensorresponding to low ATP levels and can be activated by Metformin (MF). MF is adiabetes drug that can modulate several pathways switching Mo activation. Wehave previously reported that pretreatment of bone marrow derived macrophages(BMDM) with MF prevents intracellular parasite replication and modulates theexpression of costimulatory and inhibitory molecules in peritoneal and spleenmacrophages of T.cruzi infected mice. To investigate the relevance of AMPK inPeritoneal Mo (PEMs) during T.cruzi infection, we determine the frequency of p-AMPK+ in Large PM (LPM) and Small PM (SPM) by Flow Cytometry (FC) fromBalb/c mice infected with 500 trypomastigotes (Tp) at different time points. Weobserved a significant decrease (p