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Smoking causes a dose-dependent increase in granulocyte-bound L-selectin

Authors
Journal
Thrombosis Research
0049-3848
Publisher
Elsevier
Publication Date
Volume
106
Issue
1
Identifiers
DOI: 10.1016/s0049-3848(02)00082-8
Keywords
  • Smoking
  • Neutrophils
  • L-Selectin
  • Adhesion Molecules
  • Platelets
Disciplines
  • Medicine

Abstract

Abstract The mechanism by which cigarette smoking promotes atherosclerosis remains unclear but may involve the endothelium and leukocytes. We postulated a direct acute effect of cigarette smoking on the endothelium and granulocytes by measuring granulocyte expression of L-selectin (flow cytometry) and serum L- and E-selectin (ELISA) before and after smoking in 12 smokers with peripheral vascular disease (claudicants) and 12 otherwise healthy controls. Mean (S.D.) granulocyte L-selectin, expressed as mean fluorescence intensity (MFI), increased in a dose-dependent fashion from 3.58±0.67 and 3.27±0.67 in controls and claudicants, respectively, to 3.77±0.75 and 3.49±0.79 10 min after smoking two cigarettes ( p<0.002), and to 4.11±0.95 and 3.67±0.88 30 min after four cigarettes ( p<0.001). Serum L-selectin was lower in claudicants at all time points throughout the study period compared with controls ( p<0.005) but neither serum E- nor L-selectin levels changed following smoking. Smoking led to an increase in granulocyte expression of L-selectin, which may be important in granulocyte/endothelial adhesion and thus related to atherosclerosis. The lower serum L-selectin levels in claudicants, and the absence of a rise in serum adhesion molecules on smoking, suggests consumption by activated endothelial receptors that may be part of a negative feedback mechanism.

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