Adhesion molecules and their ligands in nasal polyps of aspirin-hypersensitive patients

Background Chronic inflammation with tissue eosinophilia plays a key role in the pathogenesis of asthma and nasal polyps in patients with aspirin hypersensitivity. Objective To evaluate the expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) and their ligands (the integrins lymphocyte function-associated antigen 1 and very late-activation antigen 4 [VLA-4]) in nasal polyps of patients with aspirin hypersensitivity compared with aspirin-tolerant individuals. Methods Immunohistochemical studies were performed using a peroxidase method and monoclonal antibodies on 6-μm-thick cryostat sections cut from frozen polyps collected during elective surgery from 21 aspirin-sensitive and 23 aspirin-tolerant patients. Results The mean ± SD values of the semiquantitatively evaluated immunoexpression of ICAM-1, VCAM-1, and VLA-4 were significantly increased in patients with aspirin hypersensitivity compared with aspirin-tolerant patients (1.7 ± 0.8 vs 0.9 ± 0.8, P P P P = .57). We found a correlation between the immunoexpression of VCAM-1 and its ligand VLA-4 in all studied tissue samples ( r = 0.4; P Conclusions In nasal polyps of aspirin-hypersensitive patients, up-regulation of the adhesion molecules ICAM-1 and VCAM-1 and the integrin VLA-4 may play an important role in the development of chronic eosinophilic inflammation.