Hormesis mediated by IL-1b protects pancreatic b-cells from dysfunction and death induced by inflammatory cytokines

SÉTULA C.; ORELLANO MS; ARGAÑARÁS M.; ANDREONE L.; PERONE MJ.

Mar del Plata.

Congreso; Reunion Anual de Sociedades de Biociencias; 2023

SAIC, SAB, AAFE, AACYTAL

Both type 1 and type 2 diabetes share islet inflammation. Hormesis is aphenomenon by which a harmful substance administered to an organism in smalldoses provides resistance to subsequent contacts with higher doses.We aimed to assess if physiological concentrations of IL-1b induce hormesisleading to adaptive mechanisms, safeguarding b-cells against the characteristicinflammatory environment of diabetes.We employed INS-1E insulinoma and pancreatic islets and measured NO byGriess, viability (MTT), death (Hoechst/PI, microscopic fluorescence; Annexin V-PE/7-AAD, flow cytometry), mRNA by RT-qPCR, NF-kB (immunofluorescence)and insulin (ELISA). GSIS (glucose-stimulated insulin secretion) index wascalculated as the ratio of insulin released during 1h under stimuli of 20mM/2mMglucose. Hormesis was induced by incubation with 10 pg/ml IL-1b for 72h (IL-1blow). Cytokine-induced damage was triggered by 100 pg/ml IL-1b + 5 ng/ml IFNgfor 16h (CYT).Hormesis induced by IL-1blow protects INS-1E from the decrease in mitochondrialreduction potential triggered by CYT, diminishes cell death (p