PARTICIPATION OF THE OXIDATIVE STRESS IN THE IMMUNE ALTERATION IN BALB/C AND C57 DIABETIC MICE

ROXANA RUBINSTEIN; ROMINA ALBARRACÍN; MIRIAM WALD; ANA MARÍA GENARO

Rosario, Santa Fé, Argentina

Congreso; XLI Reunión Anual de la Sociedad Argentina de Farmacología Experimental; 2009

Sociedad Argentina de Farmacología Experimental

An increased susceptibility to infection was described in diabetic patients suggesting an immunosuppression, being hyperglycemia the main factor involved. However, there are diabetic patients with normal evolution after an infection challenge. Among the factors that can regulate this susceptibility is the balance between pro- and anti- inflammatory cytokines, type TH1 and TH2 respectively. Here we studied the effect of diabetic state in the immune response in TH1-biased C57Bl/6 (C57) 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 C57 mice. However, glucose levels in diabetic mice were significantly higher in C57 than in BALB/c. 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 (HG) but not in C57. HG diminished cell viability and increased apoptosis of BALB/c lymphocytes but not in C57. Along with this decrease in lymphocyte proliferation, an increase in oxidative stress was observed, suggesting its participation in the observed effects. Moreover, antioxidants reverted HG actions on cell viability and T and B proliferative response. These results indicate that genetic control of TH1-TH2 balance could affect the evolution of infection in subject with diabetes.