EXPRESSION OF ENDOTHELIAL AND LEUKOCYTE ADHESION MOLECULES INTERCELLULAR-ADHESION MOLECULE-1, E-SELECTIN, AND VASCULAR CELL-ADHESION MOLECULE-1 IN THE BRONCHIAL-MUCOSA IN STEADY-STATE AND ALLERGEN-INDUCED ASTHMA

Background. Interactions between cell adhesion molecules and their ligands are an integral part of inflammatory processes and may have direct relevance to the pathology of asthma. Methods: Immunostaining with antibodies to cell adhesion molecules was performed on bronchial biopsy specimens from persons with intrinsic and extrinsic asthma, normal nonasthmatic control subjects, and patients with asthma after allergen challenge. Results: There was constitutive expression of intercellular adhesion molecule-1 (ICAM-1), E-selectin and vascular celt adhesion molecule-1 (VCAM-1) in patients with intrinsic and extrinsic asthma and in control subjects. Compared with control subjects, ICAM-1 and E-selectin staining in the submucosa was greater in the intrinsic asthmatic group for intensity (p < 0.02, p < 0.05) and extent (p < 0.01, p < 0.05) of staining, respectively. No differences were observed between patients with extrinsic asthma and normal control subjects, and VCAM-1 expression did not differ among the groups. Epithelial expression of ICAM-1 was more frequent in patients with asthma compared with normal control subjects (p< 0.05). Compared with diluent challenge, bronchial biopsy specimens obtained 24 hours after allergen challenge revealed no significant differences in intensity or extent of staining for ICAM-1, E-selectin, or VCAM-1. After allergen challenge, the intensity and extent of both VCAM-1 and ICAM-1 expression correlated significantly with the number of eosinophils (cells positive for major basic protein). Epithelial ICAM-1 expression was more frequently observed after allergen challenge than after diluent challenge (p< 0.02). Conclusions: The data suggest a complex pattern of regulation for ICAM-1, E-selectin, and VCAM-1 in vivo, where they may reflect the degree of ongoing inflammation in asthma.