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,
*
First Department of Internal Medicine, Gunma University School of Medicine,
Faculty of Health Sciences, and
Laboratory of Signal Transduction, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan; and
Central Research Laboratories, Dainippon Ink and Chemicals, Sakura, Japan
Although mast cells accumulate within the mucosal epithelial layer
of patients with allergic rhinitis and bronchial asthma, the
responsible chemotactic factors are undefined. We investigated whether
mast cells sensitized with Ag-specific IgE migrate toward the Ag. MC/9
mast cells sensitized with anti-DNP IgE migrated toward
DNP-conjugated human serum albumin. This migration was
directional, and the degree was stronger than that induced by stem cell
factor. IL-3 and stem cell factor-dependent cultured mast cells derived
from mouse bone marrow also migrated toward the Ag. Subsequent
migration mediated by the Fc
RI was significantly inhibited by
incubating the cells with Y-27632, a Rho-associated coiled-coil-forming
protein kinase inhibitor, or with SB203580, a p38 mitogen-activated
protein kinase (MAPK) inhibitor. Both p38 MAPK and MAPK-activated
protein kinase (MAPKAPK)2 were activated following FcRI
aggregation, and activation of MAPKAPK2 was almost completely inhibited
by 10µM SB203580. Wortmannin or a low concentration of SB203580
partially inhibited MAPKAPK2, but did not block mast cell migration. In
contrast, Y-27632 did not affect the activation of MAPKAPK2. These
results indicate that Ag works not only as a stimulant for allergic
mediators from IgE-sensitized mast cells, but also as a chemotactic
factor for mast cells. Both p38 MAPK activation and Rho-dependent
activation of Rho-associated coiled-coil-forming protein kinase may be
required for FcRI-mediated cell migration.
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