Rosiglitazone influences the expression of leukocyte adhesion molecules and CD14 receptor in type 2 diabetes mellitus patients

• Published in: Physiological research Vol. 63 Suppl 2; pp. S293 - S298
• Main Authors: Štulc, T, Svobodová, H, Krupičková, Z, Doležalová, R, Marinov, I, Češka, R
• Format: Journal Article
• Language: English
• Published: Czech Republic Institute of Physiology 01-01-2014
• Subjects: Aged; Antigens; Atherosclerosis; Biomarkers - blood; Blood Glucose - drug effects; Blood Glucose - metabolism; Case-Control Studies; Cell adhesion & migration; Cell Adhesion Molecules - blood; Cholesterol; Cloning; Diabetes; Diabetes Mellitus, Type 2 - blood; Diabetes Mellitus, Type 2 - drug therapy; Diabetes Mellitus, Type 2 - immunology; Disease; Down-Regulation; Female; Humans; Hyperglycemia; Hypoglycemic Agents - therapeutic use; Inflammation Mediators - blood; Laboratories; Lipopolysaccharide Receptors - blood; Male; Middle Aged; Studies; Thiazolidinediones - therapeutic use; Treatment Outcome; Triglycerides
• ISSN: 0862-8408; 1802-9973
• DOI: 10.33549/physiolres.932791

Diabetes mellitus is associated with increased inflammatory response, which may contribute to atherosclerosis progression. Experimental results demonstrated anti-inflammatory activity of glitazones; their effect on leukocyte adhesion molecules has not been studied to date. We therefore studied the effect of rosiglitazone treatment on leukocyte surface expression of adhesion molecules in patients with type 2 diabetes mellitus and compared our results with findings in healthy subjects. 33 subjects with type 2 diabetes and 32 healthy controls were included; patients were examined at baseline and after 5 months of rosiglitazone treatment (4 mg/d). Leukocyte expression of adhesion molecules LFA-1, CD18 and ICAM-1 was quantified using flow cytometry; in addition, CD14 (lipopolysaccharide receptor) expression was analyzed as a marker of nonspecific immunity. The expression of examined molecules at baseline was higher in patients compared to controls. Despite only mild decrease in blood glucose, rosiglitazone treatment induced substantial decrease of CD18 and CD14 expression and borderline decrease of LFA-1 and ICAM-1 expression (on monocytes only). We thus observed improvement in the expression of leukocyte inflammatory markers after rosiglitazone treatment. This effect is supposed to be mediated by direct effect of rosiglitazone on PPAR-gamma receptors on leukocytes.