Thrombin stimulation of human coronary artery endothelial cells (HCAEC) results in the release of choline lysophospholipids (lysophosphatidylcholine, lysoPtdCho and lysoplasmenylcholine, lysoPlsCho). These amphiphilic metabolites are implicated in arrhythmogenesis following myocardial ischemia, but studies examining their direct effects on the vasculature remain limited. We and others have shown that thrombin and lysoPtdCho can increase cell surface adhesion molecules and adherence of circulating inflammatory cells to the endothelium. Our hypothesis is that these changes may be mediated, at least in part, by lysoPlsCho, thus implicating this metabolite as an inflammatory mediator. Apical stimulation of HCAEC with thrombin resulted in the production and release of choline lysophospholipids from the apical surface of the HCAEC monolayer. Basolateral stimulation had no effect on choline lysophospholipid production or release from either the apical or basolateral surface of the HCAEC monolayer. Incubation of HCAEC with lysoPlsCho or lysoPtdCho resulted in similar increases in HCAEC surface expression of P-selectin and E-selectin. Further, lysoPlsCho increased cell surface expression of P-selectin, E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) with a similar time course to that of thrombin stimulation. Increased presence of cell surface adhesion molecules may contribute to the significant increase in the adherence of neutrophils to either thrombin or lysoPlsCho stimulated HCAEC. These results demonstrate that the presence of thrombin at sites of vascular injury in the coronary circulation, resulting in increased choline lysophospholipid release from the HCAEC apical surface, may propagate vascular inflammation by upregulation of adhesion molecules and recruitment of circulating inflammatory cells.