Human lung mast cell and eosinophil adhesion to bronchial epithelium

Asthma is initiated at the mucosal surface upon aeroallergen exposure and mast cell activation. Release of eosinophil cationic proteins is thought to be responsible for epithelial damage. In this study, human peripheral blood eosinophil and human lung mast cell (HLMC) adhesion to bronchial epithelium were investigated. A high proportion of HLMC adhered to epithelial cell monolayers compared to eosinophils. In both cases, adhesion was cation-independent, and was not inhibited by function-blocking ICAM-1 mAb, despite increased basal epithelial ICAM-1 expression upon cytokine activation.;HLMC adhesion was not modulated by function blocking mAb to cell adhesion molecule families, preincubation with carbohydrates, HLMC activation (SCF or TGF-P), or epithelial activation (cytokines). A significant reduction in adhesion was observed upon pretreatment with anti-IgE, pronase, -galactosidase or endo--N-acetylgalactosaminidase (HLMC) or 4% paraformaldehyde (epithelium). No evidence for galectin involvement in adhesion was observed.;Eosinophil adhesion to alveolar epithelium was not modulated by eosinophil activation with PAF. Adhesion to bronchial epithelium was enhanced upon activation of both eosinophils (Mn2+) and epithelium (cytomix). A proportion of the enhanced adhesion was 2 (CD 18) integrin-mediated.;In conclusion, the adhesion mechanisms of mast cells and eosinophils to bronchial epithelium were different, possibly relating to their divergent in vivo functions. The differences in proportions of adherent mast cells and eosinophils to bronchial epithelium during asthma may result in the widely documented lack of mast cells compared to eosinophils in sputum and BAL in vivo.