Participation of genetic control of the Th1 –Th2 balance in diabetes-induced immune alteration.

MARA ROXANA RUBINSTEIN GUICHÓN; ANA MARÍA GENARO; MIRIAM RUTH WALD

CABA, Argentina

Congreso; III Iberoamerican Congress on Neuroimmunomodulation; 2009

Diabetes predispose to infections supporting an association with immunosuppression, being the hyperglycemia the main factor involved. However, some individuals with diabetes have poorer outcomes or complicated course after infection but others have a normal evolution. Genetic control of the Th1–Th2 balance has been associated to different resistance to infection. Here we studied the effect of diabetic state in the immune response in Th1-biased C57Bl/6 mice and Th2-biased BALB/c mice. Diabetes resulted in a decrease of Con A T-cell and LPS B-cell stimulated proliferation in BALB/c but not in C57Bl/6 mice. However, glucose levels in diabetic animals were significantly higher in C57Bl/6 than in BALB/c mice. The direct effect of elevated extracellular glucose on lymphoid cells by culturing T and B lymphocytes was investigated. Results indicate that T and B-cell proliferation in BALB/c was decreased by high concentration of glucose but not in C57Bl/6. In parallel with the decrease in lymphocyte proliferation, an increase in oxidative stress -measured as lipid peroxidation levels and reactive oxygen species production- was observed, suggesting its participation in the observed effects. These results indicate that genetic control of Th1-Th2 balance could affect the evolution of infection in subject with diabetes.