Background:
@EN 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 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.
@ES Methods:
@EN 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.
@ES Results:
@EN The expression of E-selectin was minimal in both control mucosa and nasal polyps (median: 2%, 6% respectively). Intercellular adhesion moelcule-1 (ICAM-1) showed constitutive expression on the control mucosa as well as in the 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 melecule-1 (VCAM-1) was moderately expressed on the vessels of control
mucosa
and nasal polyps (median: 16%, 23% respectively) without significant difference between the two groups. Eosinophil counts per mm* of tissue were significantly higher in the polyps than in the control mucosa (median: 82 vs 0, p<0.01) and revealed
correlation with VCAM-1 expression (p<0.05).
@ES Conclusion:
@EN These data suggest that cosinophils play an important role in the pathogenesis of nasal polyps. Among three representative vascular endothelial 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 transmigration of extravasated cells into the nasal secretion. (Korean J Otolaryngol 38:7, 1995)
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