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Mediators of Inflammation
Volume 2005 (2005), Issue 3, Pages 175-179
http://dx.doi.org/10.1155/MI.2005.175

Serum Levels of the MCP-1 Chemokine in Patients With Ischemic Stroke and Myocardial Infarction

1Department of Immunology, Palacký University Olomouc, Olomouc 77520, Czech Republic
2Institute of Molecular Biology of the National Academy of Sciences of Armenia, Yerevan, Armenia
3Department of Internal Medicine I, Palacký University and Faculty Hospital Olomouc, Olomouc 77520, Czech Republic

Received 4 February 2005; Accepted 22 February 2005

Copyright © 2005 Hindawi Publishing Corporation

Abstract

Chemokine-driven migration of inflammatory cells has been implicated in pathogenesis of atherosclerosis-associated conditions such as ischemic stroke and myocardial infarction. In this study, a candidate chemokine, monocyte chemoattractant protein (MCP)-1, was investigated in patients with both aforementioned manifestations of atheroslerotic inflammation. MCP-1 levels in serum were determined by ELISA in 40 healthy, control subjects (C), 40 patients with ischemic stroke (IS), and in 64 patients with myocardial infarction (MI). Statistical analysis utilised Mann-Whitney test, Fisher's exact test, and Spearman's rank correlation (P<.05). In comparison to control subjects (C; median/interquartile range: 239/126 pg/mL), MCP-1 serum levels were increased in both investigated patient cohorts (IS: 384/370, P<.001; MI: 360/200, P<.002). There was a substantial variability of MCP-1 serum levels, especially in the IS group. No relationship was observed between chemokine levels and atherosclerosis risk factors (hypertension, diabetes, smoking, and alcohol consumption), and MCP-1 was also not related to age or gender. Elevation of MCP-1 in circulation of patients with atherosclerosis-associated complications implicates this CC chemokine ligand (CCL)2 in inflammatory processes, which contribute to pathogenesis of myocardial infarction and ischemic stroke. Further investigations, including patient stratification, are however necessary to evaluate if MCP-1 can be utilised for clinical management of patients with these diseases.