VCAM‐1 (vascular cell adhesion molecule‐1) is a cytokine‐in‐ducible adhesion molecule which is known to mediate adhesion of mononuclear cells to endothelial cells in vitro via binding to the integrin VLA‐4 (very late antigen‐4). To further elucidate the role and regulation of VCAM‐1 in vivo, we compared in vitro and in vivo expression of VCAM‐1 in response to cytokines and investigated immunohistochemically the expression of VCAM‐1 in three murine models of experimental inflammation. These models differed with regard to the pathogenetic mechanism and the subsequent infiltrate: allergic contact dermatitis (ACD) to DNFB as a T cell‐controlled, DTH type of inflammation, cutaneous infection with Leishmania major as a chronic granulomatous inflammation and the cauterized cornea as a model for acute inflammation. VCAM‐1 was found to be markedly enhanced on vascular endothelia in all types of inflammation and after subcutaneous administration of LPS and TNF‐a. Administration of IL‐4, however, failed to induce VCAM‐1 both in vivo and in vitro. The increased VCAM‐1 expression in the inflammatory models correlated with the appearance of infiltrating monocytes/ macrophages. A concomitant influx of CD4‐positive/CD8‐positive lymphocytes was only observed in ACD and Leishmaniasis.