Nasal allergen provocation induces adhesion molecule expression and tissue eosinophilia in upper and lower airways

Background: Allergic rhinitis (AR) and asthma are characterized by means of a similar inflammatory process in which eosinophils are important effector cells. The migration of eosinophils from the blood into the tissues is dependent on adhesion molecules. Objective: To analyze the aspects of nasobronchial cross-talk, we studied the expression of adhesion molecules in nasal and bronchial mucosa after nasal allergen provocation (NP). Methods: Nine nonasthmatic subjects with seasonal AR and 9 healthy control subjects underwent NP out of season. Bronchial and nasal biopsy specimens were taken before (T-0) and 24 hours after NP (T-24). Mucosal sections were analyzed for the presence of eosinophils, IL-5, eotaxin, intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), E-selectin, and human endothelium (CD31). Results: At T-24, an influx of eosinophils was detected in nasal epithelium (P = .01) and lamina propria (P < .01), as well as in bronchial epithelium (P = .05) and lamina propria (P < .05), of the patients with AR. At T-24, increased expression of ICAM-1, as well as increased percentages of ICAM-1(+), VCAM-1(+), and E-selectin(+) vessels, were seen in nasal and bronchial tissue of patients with AR. The number of mucosal eosinophils correlated with the local expression of ICAM-1, E-selectin, and VCAM-1 in patients with AR. Conclusion: This study shows that NP in patients with AR results in generalized airway inflammation through upregulation of adhesion molecules.