Neutrophil surface expression of CD11b and CD62L in diabetic microangiopathy.
The aims of the study are (1) assessment of cell surface expression of adhesion molecules CD11b and CD62L on peripheral blood neutrophils in patients with type 2 diabetes and microangiopathy; (2) analysis of serum levels of soluble adhesion molecules: E-selectin (sE-selectin), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1) and von Willebrand factor (vWF) and; (3) evaluation of systemic inflammatory markers like interleukin-6 (IL-6), soluble interleukin-6 receptor (IL-6Rs), high sensitivity C-reactive protein (hsCRP) and fibrinogen. Thirty patients with type 2 diabetes and microangiopathy were enrolled in the study. The study group was compared to 22 patients with type 2 diabetes without microangiopathic compliations. The control group included 20 healthy volunteers. Flow cytometry was used to analyse surface expression of adhesion molecules. Both inflammatory markers and soluble adhesion molecules were determined by immunoenzymatic assay. A significant increase in neutrophil surface CD11b expression (P < 0.01) as well as decrease in surface CD62L expression (P < 0.01) were observed in the group with diabetic microangiopathy in comparison with diabetic group without microangiopathic complications and healthy controls. Moreover, significantly higher concentrations of sICAM-1 (P < 0.05), sVCAM-1 (P < 0.05), sE-selectin (P < 0.05), vWF (P < 0.01), hsCRP (P < 0.01), IL-6 (P < 0.01) and fibrinogen (P < 0.001) were also found in patients with microangiopathy in comparison with the control group. IL-6Rs concentrations did not significantly vary between groups. We concluded (1) diabetic microangiopathy is accompanied by increase in CD11b expression and decrease in CD62L expression on peripheral blood neutrophils; (2) in diabetic microangiopathy rise in CD11b expression indicates neutrophil activation and intensified adhesion; (3) the development of diabetic microangiopathy is accompanied by an increase in soluble adhesion molecules and inflammatory markers concentrations in the blood.
Mastej
K
K
Department of Angiology, Hypertension and Diabetology, Wrocław Medical University, Borowska 213, 50-556, Wrocław, Poland. kmastej@interia.pl
Adamiec
R
R
D000328:Adult; D000368:Aged; D000954:Antigens, Surface / Q000378:metabolism; D002097:C-Reactive Protein / Q000032:analysis; D039481:CD11b Antigen / Q000378:metabolism*; D015815:Cell Adhesion Molecules / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000378:metabolism / Q000473:pathology; D003925:Diabetic Angiopathies / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D003928:Diabetic Nephropathies / Q000097:blood / Q000378:metabolism / Q000473:pathology; D003930:Diabetic Retinopathy / Q000097:blood / Q000378:metabolism / Q000473:pathology; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D019041:L-Selectin / Q000378:metabolism*; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism* / Q000473:pathology
D000954:Antigens, Surface; D039481:CD11b Antigen; D015815:Cell Adhesion Molecules; C509295:ITGAM protein, human; D015850:Interleukin-6; D019041:L-Selectin; D002097:C-Reactive Protein