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Human lung mast cells (HLMC) lie in close proximity to the bronchial epithelium in asthma and adhere with high affinity to bronchial epithelial monolayers in vitro. We investigated the consequences of this adhesive interaction on HLMC activation in response to FcεRI cross-linking.Human lung mast cells were cultured with the bronchial epithelial cell line BEAS-2B or plastic control for either 30 min or 16 h and then activated with anti-IgE. Histamine was measured by radioenzymatic assay.After co-culture for 30 min, IgE-dependent histamine release from HLMC was identical on both BEAS-2B and plastic. After 16 h of co-culture, there was a marked decrease in constitutive and IgE-dependent histamine release from HLMC cultured on BEAS-2B compared with those cultured on plastic or fibronectin. In contrast, the Ca2+/ATPase inhibitor thapsigargin produced concentration-dependent histamine release that was significantly increased on BEAS-2B compared with plastic. IgE-dependent degranulation was not significantly affected by BEAS-2B-conditioned medium.BEAS-2B bronchial epithelial cells attenuate IgE-dependent but not thapsigargin-induced histamine release from HLMC. The differential effect with anti-IgE compared with thapsigargin suggests that the mechanism includes interference with the proximal FcεRI signalling pathway.