Background：Infection and allergy had been suggested to be the underlying causes of nasal polyps. Continuous inflammatory reaction from either of the two causes might result in cellular event of polyp formation. Interactions between vascular endothelial adhesion molecules and their receptors on the surface of leukocytes are an integral part of inflammatory process and may have direct relevance to the pathology of nasal polyps. The aim of this study is to understand the role of endothelial adhesion molecules and eosinophils in the pathogenesis of nasal polyps.

Methods : Immunostaining with antibodies against vascular adhesion molecules and modified Wright's stain for eosinophils were performed on the nasal polyps(polyp group) and inferior turbinate mucosa of nonallergic, noninfectious controls(control group), and compared two groups for the expression of adhesion molecules and counts of eosinophils.


Results
: The expression of E-selectin was minimal in both control mucosa and nasal polyps (median : 2%, 6% respectively). Intercellular adhesion moelcule-1(1CAM-1) showed constitutive expression on the control mucosa as well as in nasal polyps where significantly higher expression was observed both in the vessels(median : 39% vs 60%, p=0.02) and in the epithelial cells(median :6 vs 16, p=0.002). Vascular cell adhesion molecule-1(VCAM-1) was moderately expressed on the vessels of control mucossa and nasal polyps(median : 16%, 23% respecitvely) without significant difference between the two groups. Eosinophil counts per mm2 of tissue were significantly higher in the polyps than in the control mucosa(median : 82 va 0, p<0.01) and revealed correlation with VCAM-1 expression(p<0.05).


Conclusion
: These data suggest that eosinophils play an important role in the pathogenesis of nasal polyps. Among three representative vascular enddothelial adhesion molecules, ICAM-1, which is significantly upregulated on the vascular endothelial cells, might contribute to the polyp formation by recruiting inflammatory cells including eosinophils from the vascular lumen to the site of inflammation. Significant upregulation of ICAM-1 on the basal cell layer of epithelium of nasal polyps supports the mechanism of transmigraion of extravasated cells into the nasal secretion.