Effect of hyperglycemia and cortisol-mediated stress on inflammatory response and PPARγ expression of macrophages derived from thp1 line stimulated with Mtb

FERNANDEZ R; DIAZ A; D´ATTILIO L; BONGIOVANNI B; BOTTASSO O; BAY ML

Buenos Aires

Congreso; Reunión conjunta de Sociedades de Biociencias y 65ta Reunión de la SAI; Buenos Aires, 13-17 Noviembre 2017; 2017

Reunión Conjunta de Sociedades de Biociencia

Tuberculosis (TB) is the second leading cause of death by an infectious agent, Mycobacterium tuberculosis (Mtb). In 2015, WHO reported 10.4 million new TB cases, 15% of them attributed to co-morbidity TB plus type 2 diabetes mellitus (T2DM). It is estimated that 10% of the population is infected with Mtb and diabetes may increase 3 times the possibility of developing active TB. Previously we reported that patients with the TB+T2DM comorbidity showed a more pronounced adverse immune-endocrine profile than those with TB alone.In light of these results we decided to investigated the effect of hyperglycemia [D-Glucose ?Glc- 5 mM (physiological dose) or 10, 20 or 40 mM (supraphysiological doses)] and stress (cortisol 0.1 or 1 μM) on innate immune responses, i.e., the production of IL-1β (ELISA) and the expression levels of mRNA PPARγ (RT-qPCR) in 24 h cultured macrophages (Mø) derived from THP1 cell line stimulated with Mtb (strain H37Rv killed by γ radiation ?Mtbi).Mtbi stimulation significantly increased IL-1β levels regardless of Glc doses added to the cultures (p