Aspirin prevents adhesion of T lymphoblasts to vascular smooth muscle cells.

In the development of atherosclerosis, inflammatory cells adhere to and migrate into the vascular walls by interacting with vascular smooth muscle cells. To investigate the mechanism of aspirin's anti-atherogenic activity, we examined whether aspirin inhibits the adhesion of lymphocytes to human aortic smooth muscle cells (AoSMC). Aspirin inhibited T-cell adhesion to AoSMC activated by interleukin 1beta (IL-1beta) in a dose-dependent manner. Antibodies to the adhesion molecules ICAM-1 or VCAM-1, but not to E-selectin, prevented T-cell adhesion. ICAM-1 and VCAM-1 expression stimulated by IL-1beta was reduced by the treatment with aspirin, whereas the expression of E-selectin was unaffected. Nuclear factor kappaB (NF-kappaB) activity was enhanced by IL-1beta and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-kappaB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1beta-activated AoSMC by reducing NF-kappaB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.