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Biochem Biophys Res Commun. 2008 Dec 5;377(1):321-5. doi: 10.1016/j.bbrc.2008.10.004. Epub 2008 Oct 10.

IgE-induced degranulation of mucosal mast cells is negatively regulated via nicotinic acetylcholine receptors.

Author information

1
Department of Bioscience, Division of Gastrointestinal Pathophysiology, Institute of Natural Medicine, University of Toyama, Sugitani, Toyama, Japan. natsuko@inm.u-toyama.ac.jp

Abstract

The autonomic nervous system is known to mediate mast cell activation. We investigated expression of nicotinic acetylcholine receptors (nAChRs) in mucosal-type mast cells and their contribution to the regulation of mast cell activation. Expression of mRNA of nAChR alpha4, alpha7, and beta2 subunits were detected in specially differentiated mucosal-type murine bone marrow-derived mast cells (mBMMCs). Pretreatment with non-specific nAChRs agonists, acetylcholine, nicotine and epibatidine and a specific alpha7 subunit agonist GTS-21 significantly inhibited antigen-induced degranulation of mBMMCs in a dose-dependent manner and GTS-21-induced inhibition was significantly blocked by alpha7 subunit antagonist, alpha-bungarotoxin. Furthermore, confocal microscopy also demonstrated surface binding of alpha-bungarotoxin on mBMMCs. Our findings indicate that mucosal mast cell activation may be negatively regulated mainly through nAChR alpha7 subunit, suggesting that nAChRs are involved in neuronal-mucosal mast cell interactions.

PMID:
18848921
DOI:
10.1016/j.bbrc.2008.10.004
[Indexed for MEDLINE]

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