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ORIGINAL RESEARCH COMMUNICATION |
1 From the Department of Internal Medicine, Hospital Clinic, Institut d'Investigació Biomèdica August Pi i Sunyer (IDIBAPS), University of Barcelona, Spain (EB, ES, JF-S, JMN, EA, AU-M, and RE); the Consorzio Mario Negri Sud, Santa Maria Imbaro (DR); and the Università Cattolica, Campobasso, Italy (GdG)
Background: Moderate alcohol consumption protects against ischemic heart disease, possibly through an antiinflammatory effect. However, little is known about the mechanisms by which alcohol may interfere in the development of atherosclerosis.
Objective: We analyzed the effects of 2 alcoholic beverages with high (red wine) or low (gin) polyphenolic content on human monocyte adhesion to an endothelial cell line (Ea.hy926).
Design: This was a randomized, crossover trial with 8 healthy men. After a washout period, the subjects received 30 g ethanol/d as red wine or gin for 28 d. Before and after each intervention, a dietary survey and laboratory analysis were performed. Adhesion of human monocytes to endothelial cells was measured in basal and stimulated [by tumor necrosis factor 
(TNF-)] conditions. Adhesion molecules involved in monocyte-endothelium interactions were determined on the cell surface.
Results: The mean expression of very late activation antigen 4 on monocytes significantly decreased after red wine intake [by 18% (95% CI: 33%, 3%); P = 0.022]. Monocyte adhesion significantly increased after TNF- stimulation of endothelial cells. This increase, however, was 39% less (95% CI: 48%, 35%; P = 0.049) after gin intake than after the respective washout period and was nearly abolished by red wine intake [96% less than after the respective washout period (95% CI: 142%, 76%); P < 0.001]. The reduction after red wine intake was significantly different from that after gin intake (P = 0.014).
Conclusions: TNF--induced adhesion of monocytes to endothelial cells was virtually abolished after red wine consumption but was only partially reduced after gin consumption. This effect may be due to the down-regulation of adhesion molecules on the monocyte surface.
Key Words: Endothelium • alcohol • monocyte adhesion • atherosclerosis • polyphenols • adhesion molecules
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