The adherence of human PMNs to nylon fibers or endothelial cells is inhibited by exposure in vitro of the phagocytic cells to PGl2. The impaired adherence is transient and correlates with a rise in intracellular levels of cyclic AMP. Similarly, stimulation of human endothelial cells with sodium arachidonate, a precursor of PGl2, leads to impaired PMN adherence. On the other hand, PGl2 failed to alter O2- release and the bactericidal capacity of the PMNs. These findings suggest that PGl2 may play a role in regulating PMN adhesiveness to endothelial cells without compromising host defense.