Abstract
Atherosclerosis is a cardiovascular disease that begins with inflammation and ends in decreased lumen diameter, occlusion and rupture if not addressed appropriately. Markers of vascular inflammation are, but not limited to, increased expression of Cell Adhesion Molecules on the vascular endothelium, recruitment of serum monocytes to the endothelium, and increases in the presence of inflammatory cytokines. Many factors can contribute to vascular inflammation and atherosclerosis, including diabetes, obesity, smoking, and genetic factors. In this report, we examine how cigarette smoke extract (CSE) contributes to the onset of vascular inflammation by (1) increasing VCAM-1 and ICAM-1 expression in endothelium in a time- and dose-dependent manner, (2) affecting cytokine expression in endothelial cells, (3) increasing monocyte adhesion to carotid endothelial cells and (4) increasing the number of monocytes that migrate across a monolayer of carotid endothelial cells.