MYCOBACTERIUM TUBERCULOSIS TRIGGERS THE GLYCOLYTIC PATHWAY IN DENDRITIC CELLS THROUGH TLR2 LIGATION

MARIANO MAIO; JOSE LUIS MARIN FRANCO; MELANIE GENOULA; JOAQUINA BARROS; MARÍA DEL CARMEN SASIAIN; LUCIANA BALBOA

Congreso; LXIX Reunión Anual de la Sociedad Argentina de Inmunología (SAI); 2021

Tuberculosis remains a major global health problem. Its causative agent, Mycobacterium tuberculosis (Mtb), is a highly successful pathogen that interferes with dendritic cells (DC) functions impairing the onset and development of adaptive immunity. Since several studies are now revealing the importance of metabolic pathways involved in DC functions, we wondered whether Mtb could regulate the glycolytic activity of DC. For this purpose, we generated monocyte-derived DC from healthy donors and stimulated them with equivalent doses of either irradiated Mtb (iMtb) or viable Mtb. Thereafter, we evaluated lactate release and glucose consumption by enzymatic assays, the expression of HIF1a, a transcription factor that promotes the glycolytic pathway, and lactate dehydrogenase A (LDHA), enzyme which catalyzes the conversion of lactate to pyruvate, by FACS and/or qPCR. We found that DC stimulated with iMtb or infected with Mtb released lactate and consumed glucose at higher rates than untreated-DC (P