IL-1 and tumor necrosis factor (TNF) are cytokines that share many overlapping functions, including induction of expression of the vascular cell adhesion molecule (VCAM) by endothelial cells. However, because most studies of cytokine induction of adhesion molecules have used human umbilical vein endothelial cells (HUVECs) and not microvascular endothelial cells, the functional significance of such observations to sites of allergic inflammation, such as the nasal mucosa, are at present unknown. We have therefore used nasal mucosa to compare the functional response of these microvascular endothelial cells with HUVECs. HUVECs or nasal mucosal explants were stimulated in vitro with varying concentrations of IL-1 or TNF for 0 to 48 hours, and VCAM mRNA and protein expression were determined by means of immunostaining and in situ hybridization. TNF and IL-1 were equivalent in their ability to induce VCAM mRNA and protein expression by HUVECs. In contrast, TNF was significantly more potent than IL-1 in inducing VCAM mRNA and protein expression by nasal mucosal microvascular endothelial cells. The recovery of significant amounts of IL-1 after incubation of recombinant IL-1 with nasal mucosa, as well as the ability of IL-1 to induce intercellular adhesion molecular expression by nasal mucosa, suggests that neither degradation of IL-1 nor downregulation of IL-1 receptors in nasal mucosa is likely to explain the inability of IL-1 to induce VCAM expression by nasal mucosa. These studies suggest that microvascular endothelial cells in the nasal mucosa differ functionally from HUVECs and that TNF may be more important than IL-1 in induction of VCAM expression in the nasal mucosa.