Summary Peroxisome proliferator-activated receptor-γ (PPAR-γ ) is a member of nuclear hormone receptor superfamily, and is known to play a role in various biological processes including inflammatory responses and adipocyte differentiation. CX3CL1/fractalkine is a potent agonist for chemotaxis and adhesion of monocytes and lymphocytes. Endothelial cells produce fractalkine when stimulated with cytokines such as interleukin-1 (IL-1), tumour necrosis factor-α and interferon-γ (IFN-γ ). We herein report that 15-deoxy-᭝ 12,14 -prostaglandin J 2 (15d-PGJ 2 ), a PPAR-γ agonist, inhibits the expression of fractalkine induced by IFN-γ or IL-1 β in human endothelial cells. Agonist for PPAR-α (WY14643) or PPAR-γ (ciglitazone) did not inhibit the cytokine-induced fractalkine expression, and the effect of 15d-PGJ 2 may be independent of PPAR. 15-Deoxy-⌬ 12,14 prostaglandin J 2 also inhibited the adhesion of blood mononuclear cells to endothelial monolayers treated with IFN-γ or IL-1 β . The data suggest that 15d-PGJ 2 regulates inflammatory reactions, at least in part, through the inhibition of fractalkine expression and leucocyte traffic through the endothelium.