title: Influence of insulin therapy on expression of chemokine receptor CCR5 and selected inflammatory markers in patients with type 2 diabetes mellitus.
abstract: OBJECTIVE
  Leukocyte migration to the subendothelial space is considered crucial in the initiation of atherosclerosis. There is increasing evidence that overexpression of chemokine receptors contribute to this process. CCR5 is one of the receptors present on peripheral T lymphocytes, monocytes and macrophages. We decided to evaluate the expression of CCR5 on monocytes and macrophages in peripheral blood and selected inflammatory markers in patients with type 2 diabetes mellitus before and after the initiation of insulin therapy.
  
  
  METHODS
  A total of 10 patients with newly diagnosed type 2 diabetes and 6 healthy control subjects were studied. Assessment of CCR5 expression on the surface of monocytes and macrophages in peripheral blood was performed using flow cytometry before the initiation of insulin therapy and after 5-week treatment. Serum concentrations of RANTES, TNF-alpha, IL-6 and hsCRP were assessed.
  
  
  RESULTS
  When compared to control subjects, we observed higher densities of CCR5 on the surface of peripheral blood monocytes and macrophages and higher concentrations of RANTES, TNF-alpha, IL-6 and hsCRP before insulin therapy. After 5-week insulin therapy, there was a significant decrease in the expression of CCR5 on the surface of these cells and a significant fall in serum levels of RANTES, IL-6, TNF-alpha and hsCRP.
  
  
  CONCLUSIONS
  Type 2 diabetes leads to an increase in the inflammatory process, and insulin therapy inhibits the early stages of this process.
authors.affiliation: Department of Internal Medicine, Metabolic Disorders and Hypertension, Karol Marcinkowski University of Medical Sciences, Szamarzewskiego 84, 61-847 Poznan, Poland. pawelbogdanski@wp.pl
authors.forename: P
authors.initials: P
authors.lastname: Bogdanski
authors.forename: D
authors.initials: D
authors.lastname: Pupek-Musialik
authors.forename: J
authors.initials: J
authors.lastname: Dytfeld
authors.forename: P P
authors.initials: PP
authors.lastname: Jagodzinski
authors.forename: A
authors.initials: A
authors.lastname: Jablecka
authors.forename: A
authors.initials: A
authors.lastname: Kujawa
authors.forename: K
authors.initials: K
authors.lastname: Musialik
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D018946:Chemokine CCL5 / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D005786:Gene Expression Regulation; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D018836:Inflammation Mediators / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology*; D015850:Interleukin-6 / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism; D019713:Receptors, CCR5 / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018946:Chemokine CCL5; D007004:Hypoglycemic Agents; D018836:Inflammation Mediators; D007328:Insulin; D015850:Interleukin-6; D019713:Receptors, CCR5; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein