Objective: The aim was to investigate whether interleukin-lβ (IL-1β) plays a role in modulating the adhesion of monocytes and neutrophils to vascular smooth muscle cells, and to identify what molecules on these cells may be involved in the adhesion. Methods: Rat aortic smooth muscle cells were challenged with IL-1β and tested for adhesion of prelabelled monocytes and neutrophils. Northern analysis, reverse transcription/polymerase chain reaction (RT/PCR), and immunocytochemical staining were used to measure the changes of intercellular adhesion molecule-1 (ICAM-1) and other adhesion molecules in response to IL-1β stimulation. Neutralising antibody against ICAM-I was used to demonstrate a role of ICAM-1 in this IL-1β induced adhesion. Results: IL-1β induced the adhesion of monocytes and neutrophils to aortic smooth muscle cells in a concentration and time dependent manner. IL-1β-induced adhesion was inhibited by preincubation of the cells with an IL-1β receptor antagonist (IL-1β). Northern analysis and RT/PCR showed that ICAM-1 mRNA represents a predominant adhesion molecule induced by IL-1β, and that the expression of ICAM-1 mRNA precedes and parallels the induced adhesion profiles of aortic smooth muscle cells for leucocytes. Immunocytochemical staining confirmed the IL-1β induced ICAM-1 expression on the smooth muscle cells. Moreover, a monoclonal anti-rat ICAM-1 antibody produced a concentration dependent inhibition of the IL-1β induced adhesion of monocytes and neutrophils to the smooth muscle cells. Conclusions: IL-1β actively regulates functional ICAM-1 expression in vascular smooth muscle cells. The IL-1β-induced expression of ICAM-1 on the smooth muscle cells may be an important contributor to the increased adhesion by monocytes and neutrophils to these cells and suggests that IL-1β might play a role in the proinflammatory and immune functions of the modified smooth muscle cells during atherosclerosis and restenosis. Cardiovascular Research 1994;28:1808-1814