Affiliations: Department of Internal Medicine, Malattie Cardiovascolari e Nefrourologiche, University of Palermo, Italy | Department of Endocrinology, University of Palermo, Italy | Department of Hematology, University of Palermo, Italy
Note: [] Corresponding author: Prof. Gregorio Caimi, Via Leonardo da Vinci, 52, 90145 Palermo, Italy. Tel.: +39 91 6554406; Fax: +39 91 6554535.
Abstract: We examined the polymorphonuclear leukocyte (PMN) integrin pattern in 45 diabetic subjects without macrovascular complications, including 21 subjects with type 1 and 24 with type 2 diabetes mellitus. The PMN adhesion molecules (CD11a, CD11b, CD11c, CD18) were evaluated using indirect immunofluorescence and a flow cytometer, at baseline and after in vitro activation with 4‐phorbol 12‐myristate 13‐acetate (PMA) and N‐formyl‐methionyl‐leucyl‐phenyl‐alanine (fMLP). At baseline, in diabetic subjects the phenotypical expression of CD11a and CD11b was significantly reduced and CD11c was increased, whereas CD18 was unchanged in comparison with normals. Considering type 1 and 2 diabetic subjects separately, CD11a was reduced and CD11c was increased in both subgroups, CD11b was decreased only in type 1 diabetics and CD18, decreased in type 1, was increased in type 2 subjects. After activation with PMA and fMLP, in normal subjects we observed a significant increase of all PMN adhesion molecules whereas in diabetic subjects only CD11c increased significantly with both activating agents, and CD11b increased only after PMA activation. In type 1 diabetic subjects only CD11c expression was increased, and in type 2 diabetic subjects an increase of CD11b (with PMA) and an increase of CD11c (with fMLP) were noted. In conclusion, we found in diabetic subjects of type 1 and 2 an altered behaviour pattern of PMN integrins both at baseline and, in particular, after in vitro activation. These data may help in explaining the role of PMN in the evolution of diabetic vascular complications.
