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Division of Respiratory Medicine, Leicester University Medical School, United Kingdom
Correspondence: Dr. Peter Bradding, Department of Respiratory Medicine, Glenfield Hospital, Groby Rd., Leicester, LE3 9QP UK. E-mail: pbradding{at}hotmail.com
Mast cells contribute to the pathophysiology of asthma through their
immunomediator-secretory activity in response to both immunological and
nonimmunological stimuli, and infiltrate the bronchial epithelium in
this disease. We hypothesized that human lung mast cells (HLMC)
localize to the bronchial epithelium via a specific cell-cell adhesion
mechanism. We investigated the adhesion of HLMC to primary bronchial
epithelial cells and the bronchial epithelial 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 cytokines,
did not require Ca2+, and was not integrin-mediated.
IgE-dependent activation of HLMC produced an approximately 40%
inhibition of adhesion. There was significant attenuation of adhesion
after incubation of HLMC with pronase, ß-galactosidase, and
endo-
-N-acetylgalactosaminidase, indicating that HLMC
adhere to bronchial epithelial cells via galactose-bearing
carbohydrates expressed on a cell-surface peptide(s).
Key Words: adhesion molecules • galactose
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