Nasal challenge with allergen upregulates the local expression of vascular endothelial adhesion molecules.

To understand the events involved in selective eosinophil migration into allergic inflammatory sites, we studied the expression of vascular endothelial adhesion molecules in the nasal mucosa. Ten subjects with asymptomatic seasonal allergic rhinitis and 13 nonallergic subjects underwent localized allergen challenge of one inferior turbinate. Twenty-four hours later, biopsy specimens were obtained from the inferior turbinates, bilaterally in the seasonally allergic subjects and unilaterally in the nonallergic control subjects. The specimens were divided, sectioned, and either stained for identification of eosinophils or analyzed immunohistochemically for intercellular adhesion molecule-1, E-selectin, vascular cell adhesion molecule-1 (VCAM-1), and von Willebrand's factor. Intercellular adhesion molecule-1 expression was observed in all mucosal specimens, with no significant difference among groups. E-selectin showed minimal baseline expression, and low levels were significantly induced on the challenged mucosa of the allergic compared with nonallergic subjects (p < 0.05). VCAM-1 was expressed basally and was significantly upregulated by allergen challenge, compared with the nonchallenged side and nonallergic control subjects (p < 0.05). Submucosal eosinophils increased significantly in allergic subjects 24 hours after antigen challenge, compared with nonallergic control subjects and weakly correlated with VCAM-1 expression (rs = 0.33, p = 0.06). Our results suggest that endothelial activation accompanies allergic inflammation. Furthermore, because the counterligand for VCAM-1, very late activation antigen-4, is present on eosinophils, VCAM-1 upregulation may contribute to the selective recruitment of these cells to the nasal mucosa.