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Cutting Edge |
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,,¶
Departments of
*
Dermatology,
Immunology, and
Atopy (Allergy) Research Center, Juntendo University School of Medicine, Tokyo, Japan; Departments of
Bacteriology and
¶ Biochemistry, Institute of Tropical Medicine, and
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Department of Applied Chemistry, Faculty of Engineering, Nagasaki University, Nagasaki, Japan; and
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Department of Molecular Cell Immunology and Allergology, Advanced Medical Research Center, Nihon University School of Medicine, Tokyo, Japan
Mucosal mast cells strategically located at the optimal site
interact with invading bacteria. Presence of VacA, the virulent
Helicobacter pylori cytotoxin, is correlated with the
severity of H. pylori-induced gastritis. To examine the
mechanisms of inflammation in H. pylori-induced
gastritis, we administered VacA to the mice. Inoculation of VacA
resulted in epithelium vacuolization and marked infiltrations of mast
cells and mononuclear cells into the mucosal epithelium within 24
h. In an in vitro study using bone marrow-derived mast cells, VacA
directly bound and showed a chemotactic activity to the mast cell. In
addition, VacA induced bone marrow-derived mast cells to produce
proinflammatory cytokines, TNF-
, macrophage-inflammatory
protein-1, IL-1
, IL-6, IL-10, and IL-13 in a
dose-dependent manner without causing degranulation. The present study
suggests that early activation of mast cells by VacA may be the host
early response to clear the bacteria and also may contribute to the
pathogenesis of H. pylori-induced
gastritis.
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