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Journal of Biochemistry 2004 136(6):741-746; doi:10.1093/jb/mvh181
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© 2004 The Japanese Biochemical Society

JB MINIREVIEWS

Helicobacter pylori Vacuolating Cytotoxin, VacA, Is Responsible for Gastric Ulceration

Akihiro Wada1,2,*, Eiki Yamasaki1,2 and Toshiya Hirayama1

1 Department of Bacteriology, Institute of Tropical Medicine, Nagasaki University, Nagasaki 8528523; and 2 PRESTO, Japan Science and Technology Corporation, Saitama 332-0012

Pathogenic strains of Helicobacter pylori produce a potent exotoxin, VacA, which causes progressive vacuolation as well as gastric injury. Most H. pylori strains secrete VacA into the extracellular space. After exposure of VacA to acidic or basic pH, re-oligomerized VacA (mainly 6 monomeric units) at neutral pH is more toxic. Although the mechanisms have not been defined, VacA induces multiple effects on epithelial and lymphatic cells, i.e., vacuolation with alterations of endo-lysosomal function, anion-selective channel formation, mitochondrial damage, and the inhibition of primary human CD4+ cell proliferation. VacA binds to two types of receptor-like protein tyrosine phosphatases (RPTP), RPTP{alpha} and RPTPß, on the surface of target cells. Oral administration of VacA to wild-type mice, but not to RPTPß KO mice, results in gastric ulcers, suggesting that RPTPß is essential for intoxication of gastric tissue by VacA. As the potential roles of VacA as a ligand for RPTP{alpha} and RPTPß are only poor understood, further studies are needed to determine the importance of VacA in the pathogenisis of disease due to H. pylori infection.

* To whom correspondence should be addressed at: Department of Bacteriology, Institute of Tropical Medicine, Nagasaki University, Nagasaki 852-8523. Tel: +81-95-849-7833, Fax: +81-95-849-7805, E-mail: a-wada{at}net.nagasaki-u.ac.jp


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