Simvastatin down-regulates the production of Interleukin-8 by neutrophil leukocytes from dyslipidemic patients

BMC Cardiovascular Disorders

Research Article

Catherine Klersy¹  Ramona C Maio²  Laura Schembri²  Luana Castiglioni²  Marco Cosentino²  Luigina Guasti²  Laura Robustelli Test²  Christian Mongiardi²  Anna Maria Grandi²  Franca Marino²  Andrea Maria Maresca² 

[1] Biometry and Clinical Epidemiology, IRCCS Policlinico S. Matteo, Pavia, Italy;Department of Clinical and Experimental Medicine, University of Insubria, Viale Borri 57, 21100, Varese, Italy;

关键词: Neutrophils;    Interleukin-8;    Dyslipidemia;    Statin;   

DOI  :  10.1186/1471-2261-14-37

 received in 2013-09-25, accepted in 2014-03-06,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundNeutrophil (PMN) leukocytes participate to the initial phases of atherosclerosis through the release of Interleukin 8 (CxCL8; IL-8) that contribute to amplification of inflammation. Aim of the study is to investigate the production of IL-8 by PMN leukocytes from dyslipidemic patients treated with simvastatin.MethodsIn 15 dyslipidemic subjects with moderately increased cardiovascular risk, assessed by Framingham Risk Score, blood samples were obtain to investigate PMNs IL-8 production [at baseline and after N-formyl-Met-Leu-Phe (fMLP) stimulation] before and after long-term (1-year) simvastatin treatment.ResultsThe resting release of IL-8 was higher in dyslipidemic patients at baseline when compared with control subjects (p < 0.05). One year of treatment was significantly associated with reduced IL-8 production (p < 0.01). Moreover, the fMLP-induced IL-8 production in dyslipidemic untreated patients was higher than that of controls (p < 0.05) and was reduced after simvastatin treatment (p < 0.01). IL-8 release after 1 year of treatment was reduced to levels which were lower than those observed in control subjects both for resting and stimulated cytokine production (p < 0.01).ConclusionsProlonged treatment with simvastatin is associated with a reduction of IL-8 production, suggesting the possibility of statin to modulate the pro-inflammatory response in PMNs of patients with moderately increased cardiovascular risk.

【 授权许可】

Unknown   
© Marino et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.