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

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.