6.2.1 Effects of hyperglycemic and cortisol-stressful conditions over galectins gene expression in cultured THP-1 –derived macrophages.

IMHOFF MATILDE; DIAB MAGDALENA; FERNÁNDEZ, ROCÍO D. V.; MASSA, ESTEFANÍA; GALLUCCI, GEORGINA; ARIANA DIAZ,; BONGIOVANNI BETTINA; BOTTASSO OSCAR; BAY MARÍA L; D'ATTILIO LUCIANO

Mar del Plata

Congreso; REUNIÓN CONJUNTA SAIC SAI&FAIC SAFIS; 2022

SAIC SAI&FAIC SAFIS

Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), continues to be among the top ten leading causes of mortality worldwide. A quarter of the world’s population is infected with Mtb and type 2 diabetes mellitus (TB+T2DM) may increase 3 times the possibility of developing active TB. We demonstrated that TB and TB+T2DM patients showed an immune-endocrine-metabolic (IEM) imbalance: elevated plasma levels of pro and anti-inflammatory cytokines as well as cortisol-Gc, along with elevated circulating levels of galectins (Gal-1 and 3). Moreover, this IEM-imbalanced environment modulates macrophage functions at the beginning of Mtb-response. To expand this knowledge, we studied the effect of glycemia [D-Glucose-Glc 5mM (physiological dose) or 10, 20, or 40 mM (supraphysiological doses-SPD)] and cortisol-induced stress (Gc-IS. 0.1 or 1μM) over the mRNA expression of Gal-1, Gal-3 and Gal-9, along with pro and anti-inflammatories transcripts (IL-1β, IL-6, and IL-10) and GLUT 1, 3 and 4 in cultured THP-1 derived macrophages stimulated with Mtbi (strain H37Rv killed by gamma radiation-Mtb). Glc SPD did not affect transcripts expression in all culture conditions, except for Gal-3 and IL-10 in stimulated cultures, which appeared increased (p