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Attenuation of human lung mast cell degranulation by bronchial epithelium
Author(s) -
Yang W.,
Wardlaw A. J.,
Bradding P.
Publication year - 2006
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.2006.01041.x
Subject(s) - histamine , degranulation , thapsigargin , immunoglobulin e , mast cell , chemistry , epithelium , immunology , medicine , pharmacology , endocrinology , biology , calcium , antibody , pathology , biochemistry , receptor
Background: 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 Fc ɛ RI cross‐linking. Methods: 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. Results: 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 Ca 2+ /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. Conclusions: 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 Fc ɛ RI signalling pathway.