Binding of monocytes from normolipidemic hyperglycemic patients with type 1 diabetes to endothelial cells is increased in vitro

Increased endothelial binding and emigration of monocytes play a dominant r ole in the pathogenesis of atherosclerosis in diabetes mellitus. Previous S tudies revealed that hyperlipidemia correlates with monocyte binding in vit ro. The aim of this study was to characterize the monocyte-endothelial inte raction of leucocytes of hyperglycemic patients with type 1 diabetes but la cking hyperlipidemia. We isolated monocytes from healthy controls and normo lipidemic type 1 diabetes patients with elevated levels of HbA(1)c and quan tified monocyte binding by an immunoillumometric cell adhesion assay. Purit y of isolated monocytes was at least 98%. Endothelial binding of monocytes from patients with type 1 diabetes was found to be significantly increased compared to controls (19.2 +/- 3.9% vs. 14.9 +/- 3.5%). This difference of monocyte binding remained unchanged if the endothelial cells were stimulate d with 27.7 mmol/l glucose for seven days prior to adhesion studies (31.5 /- 4.9% in diabetes patients. vs. 25.8 +/- 4.1% in controls) whereby monocy te binding markedly increased under these hyperglycemic conditions. Further more, an increased CD11b expression could be demonstrated on monocytes of n ormolipidemic hyperglycemic type I diabetes patients Thus we suggest that h yperglycemia per se may contribute to increased monocyte binding to endothe lial cells by promoting leucocyte integrin expression. Recently performed s tudies of our group strengthen the hypothesis that this monocyte activation is mediated by stimulation of the beta-isoform of proteinkinase C.