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During an inflammatory reaction, an increased number of circulating monocytes adhere to the endothelial cells (EC) of the vessel wall. This process is mediated by molecules located on the surface of monocytes and EC. Locally released inflammatory mediators can modulate monocyte-EC interaction. In an earlier study we reported that stimulation of monolayers of cultured venous EC with rIFN-gamma enhanced their adhesiveness for monocytes. The aim of the present study was to investigate the effect of rIFN-gamma on peripheral blood monocytes with regard to the expression of surface molecules and the binding to non-stimulated or cytokine-stimulated EC. Flow cytometric analysis demonstrated that monocytes stimulated with 500 U/ml rIFN-gamma for 24 h showed increased expression of CR3 (CD11b/CD18), p150,95 (CD11c/CD18) and Fc gamma RI (CD64); the expression of LFA-1 (CD11a/CD18), L-selectin, CD14 and VLA-4 (CD49d/CD29) did not change or was slightly reduced. Upon stimulation with rIFN-gamma monocytes showed an enhanced binding to both non-stimulated or rIFN-gamma-stimulated EC. This was even more pronounced when EC had been stimulated with rIL-1 alpha for 24 h. The increased binding of rIFN-gamma-stimulated monocytes to rIL-1 alpha-stimulated EC was further analysed. Studies with MoAbs against adhesion molecules on monocytes revealed that the binding of rIFN-gamma-stimulated monocytes, but not that of non-stimulated monocytes, to rIL-1 alpha-stimulated EC was inhibited by about 30-60% with MoAbs against CD11a, CD11b, CD18, L-selectin or CD14. MoAbs against CD11c or CD49d had little or no effect. From these results, we conclude that exposure of monocytes to rIFN-gamma enhances their adhesiveness to cytokine-stimulated EC by a mechanism which involves CD11a/CD18, CD11b/CD18, CD14 and L-selectin on monocytes.
Wang et al. (1994) studied this question.