Adhesion of human lung mast cells to bronchial epithelium: evidence for a novel carbohydrate-mediated mechanism

Mast cells contribute to the pathophysiology of asthma through their immuno mediatorsecretory activity in response to both immunological and nonimmunol ogical stimuli, and infiltrate the bronchial epithelium in this disease. We hypothesized that human lune mast cells (HLMC) localize to the bronchial e pithelium via a specific cell-cell adhesion mechanism. We investigated the adhesion of HLMC to primary bronchial epithelial cells and the bronchial ep ithelial cell line BEAS-2B. HLMC adhered avidly to both primary cultures of bronchial epithelial cells and BEAS-2B cells (mean adhesion 68.4 and 60.1% , respectively) compared with eosinophil adhesion to BEAS-2B (mean adhesion 10.3%). HLMC adhesion did not alter after epithelial activation with cytok ines, did not require Ca2+, and was not integrin-mediated. IgE-dependent ac tivation of HLMC produced an approximately 40% inhibition of adhesion. Ther e was significant attenuation of adhesion after incubation of HLMC with pro nase, beta-galactosidase, and endo-alpha-N-acetylgalactosaminidase, indicat ing that HLMC adhere to bronchial epithelial cells via galactose-bearing ca rbohydrates expressed on a cell surface peptide(s).