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

Franca Marino1, Andrea Maria Maresca1*, Luana Castiglioni1, Marco Cosentino1, Ramona C Maio1, Laura Schembri1, Catherine Klersy2, Christian Mongiardi1, Laura Robustelli Test1, Anna Maria Grandi1 and Luigina Guasti1

Author Affiliations

1 Department of Clinical and Experimental Medicine, University of Insubria, Viale Borri 57, 21100 Varese, Italy

2 Biometry and Clinical Epidemiology, IRCCS Policlinico S. Matteo, Pavia, Italy

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BMC Cardiovascular Disorders 2014, 14:37  doi:10.1186/1471-2261-14-37

Published: 15 March 2014



Neutrophil (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.


In 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.


The 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).


Prolonged 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.

Neutrophils; Interleukin-8; Dyslipidemia; Statin