ADHESION MOLECULE EXPRESSION AND THE INFLAMMATORY CELL INFILTRATE IN DELAYED PRESSURE URTICARIA

We have investigated the kinetics of the leucocyte infiltrate in delayed pressure urticaria (DPU) in relation to the in vivo expression of the cytokine-regulated cell surface adhesion molecules, E-selectin (endothelial adhesion molecule-1, ELAM-1), intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1). Immunohistochemical analysis was performed on biopsies taken from unchallenged skin, and at 0, 2, 6, 24, 48 and 120 h after weighted rods had been applied to 13 patients with DPU. There was moderate to marked upregulation of E-selectin at 6 and 24 h after application of pressure. At 24 h, more patients showed expression of VCAM-1 on perivascular cells than before pressure. Moderate expression of ICAM-1 was present in some biopsies from both unchallenged and pressure-challenged skin, but there was no clear trend. In DPU, there was a significant increase in the neutrophil count at 2 h after a pressure challenge, with further increases at 6 and 24 h. The median cell counts per high-power field of eosinophils and monocyte/macrophages increased significantly at 24 h after pressure. Biopsies from four normal controls subjected to an identical pressure challenge showed no detectable changes in adhesion molecule expression or in the cell infiltrate. The findings in four patients with chronic idiopathic urticaria not associated with DPU were qualitatively similar to (but intermediate in severity between) the findings in DPU weals at 6 and 24 h. These results suggest that vascular endothelial activation is an early response to pressure challenge in DPU, and is also present in chronic idiopathic urticaria. The inflammatory infiltrate in DPU differs in intensity, but not in composition, from that in chronic idiopathic urticaria.