Caimi G, Montana M, Citarrella R, Porretto F, Catania A, Lo Presti R
Department of Internal Medicine, Malattie Cardiovascolari e Nefrourologiche, University of Palermo, Italy.
Clin Hemorheol Microcirc. 2002;27(2):83-9.
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.
我们检测了45例无大血管并发症的糖尿病患者的多形核白细胞（PMN）整合素模式，其中包括21例1型糖尿病患者和24例2型糖尿病患者。使用间接免疫荧光法和流式细胞仪，在基线时以及用4-佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）和N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸（fMLP）进行体外激活后，评估PMN黏附分子（CD11a、CD11b、CD11c、CD18）。在基线时，糖尿病患者中CD11a和CD11b的表型表达显著降低，CD11c增加，而与正常人相比，CD18无变化。分别考虑1型和2型糖尿病患者，两个亚组中CD11a均降低，CD11c均增加，CD11b仅在1型糖尿病患者中降低，CD18在1型糖尿病患者中降低，在2型患者中增加。在用PMA和fMLP激活后，正常受试者中所有PMN黏附分子均显著增加，而在糖尿病患者中，仅CD11c在两种激活剂作用下均显著增加，CD11b仅在PMA激活后增加。在1型糖尿病患者中仅CD11c表达增加，在2型糖尿病患者中，观察到CD11b（用PMA）增加和CD11c（用fMLP）增加。总之，我们发现1型和2型糖尿病患者在基线时，尤其是在体外激活后，PMN整合素的行为模式发生改变。这些数据可能有助于解释PMN在糖尿病血管并发症演变中的作用。
