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

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

Ciudad Autómona de Buenos Aires

Congreso; XXXIX Reunión Anual de la Asociación Argentina de Farmacología Experimental (SAFE); 2007

Asociación Argentina de Farmacología Experimental

Diabetes predispose to infections supporting an association with immunosuppression, being the hyperglycemia the main factor involved. However, some individuals with diabetes have poorer outcomes after infection and increase incidence of hospital pathogen invasion 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 diabetes state in the immune response in Th1-biased C57Bl/6 (C57) mice and Th2-biased BALB/c mice. We observed that diabetes result in a time- dependent decrease of Con A T-cell and LPS B-cell stimulated proliferation in BALB/c mice. In contrast, in C57 mice diabetes did not induce inhibition of   lymphocyte reactivity. However, glucose levels in diabetic animals were significantly higher in C57 than BALB/c mice. Therefore, the direct effect of elevated extracellular glucose on lymphoid cells by culturing BALB/c and C57 mice T and B lymphocytes was investigated. Results indicate that T and B-cell proliferation in BALB/c  was decrease by high concentration of glucose but not the C57 one. Oxidative stress production, measureared as lipid peroxidation levels increased when T and B cell proliferation was diminished, 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.