Expression of E-Selectin, ICAM-1 and VCAM-1 on Bronchial Biopsies from Allergic and Non-Allergic Asthmatic Patients

摘要

The bronchial mucosa of asthmatic patients is characterized by a large influx of eosinophils, monocytes and lymphocytes. Leucocyte migration and accumulation is thought to involve adhesion molecules, as shown in an animal of allergic asthma and in humans with other allergic diseases. The aim of this study was to evaluate the expression of E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cellular adhesion molecule-1 (VCAM-1) on endothelium and epithelium in bronchial biopsies obtained from patients with allergic (n = 17) and non-allergic asthma (n = 18). Bronchial biopsies were taken in asthmatic patients and control subjects (n = 10) by fiberoptic bronchoscopy and embedded in paraffin. The cellular infiltrate was evaluated by May-Grünwald-Giemsa staining. Adhesion molecule expression was analyzed by immunohistochemistry using mouse monoclonal antibodies; the results were expressed as the percentage of positive cells. For each patient, we evaluated the severity of asthma as defined by the AAS score and the treatment. In controls, low expression of ICAM-1 was observed on the epithelium and endothelium (9.6 ± 2.7 and 11.2 ± 4.1, respectively), while E-selectin and VCAM-1 were not expressed. In patients with allergic asthma, a significant increase of ICAM-1 expression was observed on epithelium and endothelium (28 ± 5.3 and 35.6 ± 5, respectively), whereas E-selectin (17.4 ± 4.8) and VCAM-1 (12.8 ± 3.6) were overexpressed only on endothelium. In allergic asthmatic patients, adhesion molecule expression on endothelium was correlated with eosinophil and total leucocyte infiltrate (p < 0.05). In contrast, adhesion molecule expression in biopsies from patients with non-allergic asthma (14.1 ± 5.2 and 15.3 ± 3.6 for ICAM-1 expression on epithelium and endothelium, respectively) was not significantly different from the control subjects. Among the non-allergic asthmatics, those with a high leucocyte infiltrate in bronchial mucosa (n = 5) had increased expression of adhesion molecules on endothelium when compared with those exhibiting a slight infiltrate (p < 0.05 for E-selectin and VCAM-1 expression; p = NS for ICAM-1). In the group of non-allergic asthmatics, more patients were under corticosteroids (inhaled or oral treatment) than in the group of allergic asthmatics. In conclusion, ICAM-1, E-selectin and VCAM-1 expression in bronchial mucosa may be involved in leucocyte and particularly in eosinophil infiltration, an important feature of the asthmatic inflammatory