The effect of experimental diabetes on high mobility group box 1 protein expression in endotoxin-induced acute lung injury.

Abstract

The incidence and prevalence of diabetes have recently increased. Hyperglycemia, which is commonly seen in intensive care medicine, is associated with increased morbidity and mortality. For instance, diabetes is associated with altered immune and hemostatic responses. High mobility group box 1 (HMGB1) protein plays a key role in various inflammatory diseases. This study investigated the increase in lung damage due to diabetes and the rise in HMGB1 levels in a lipopolysaccharide (LPS)-induced systemic inflammation rat model. Diabetes was induced by streptozotocin infusion 4 wk prior to LPS administration, followed by measurements of blood glucose and serum cytokine levels. Separate cohorts were sacrificed 12h post-LPS administration and analyzed for lung damage. Diabetic animals had significantly higher blood glucose and enhanced lung damage. In addition, levels of serum HMGB1, tumor necrosis factor-α, and interleukin-6 were increased in diabetic rats. Diabetes may exacerbate systemic inflammation as evidenced by higher serum HMGB1 and cytokine levels and enhanced lung damage in the rat systemic inflammation model.