Aspirin prevents adhesion of T lymphoblasts to vascular smooth muscle cells

Abstract 

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 1β (IL-1β) 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-1β was reduced by the treatment with aspirin, whereas the expression of E-selectin was unaffected. Nuclear factor κB (NF-κB) activity was enhanced by IL-1β and reduced by aspirin, indicating that decreased ICAM-1 and VCAM-1 expression was due to reduced NF-κB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL-1β-activated AoSMC by reducing NF-κB activity and decreasing expression of ICAM-1 and VCAM-1, and may prevent the development of atherosclerosis.

Abbreviations: AoSMC, aortic smooth muscle cells, IL-1β, interleukin 1β, VSMC, vascular smooth muscle cells, NF-κB, nuclear factor κB, FITC, fluorescein isothiocyanate, FACS, fluorescence-activated cell sorter analysis, MFI, mean fluorescence intensity, ASA, acetyl salicylic acid

Keywords: Atherosclerosis, Anti-inflammatory activity, Aspirin, ICAM-1, VCAM-1