Effect of hyperglycemia and cortisol-mediated stress on inflammatory response and PPARγ expression of macrophages derived from THP1 line stimulated with Mtb.

FERNÁNDEZ, ROCÍO DEL VALLE; DÍAZ ARIANA; D'ATTILIO LUCIANO; BONGIOVANNI BETTINA; BOTTASSO OSCAR; BAY MARÍA L

Buenos Aires

Congreso; Reunión Conjuntas de Sociedades Biomédicas; 2017

SAI

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 investigate the effect of hyperglycemia [D-Glucose ?Glc- 5 mM (physiological dose) or 10, 20 or 40 mM (supraphysiological doses)] and cortisol-induced stress (0.1 or 1 μM) on innate immune responses, for example 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