Helicobacter pylori VacA and gastric ulcer.

VacA, the only protein toxin produced by Helicobacter pylori, vacuolates cultured cells. The presence of 2 VacA receptors has been demonstrated. One is the receptor-type protein tyrosine phosphatase (RPTP) zeta/beta (PTP zeta/beta), and the other is RPTP alpha. VacA binds to PTP zeta/beta, resulting in gastric epithelial detachment through the tyrosine phosphorylation of Git-1, which then leads to gastric ulceration by the direct action of gastric acid. Thus, disturbance of adhesion between gastric epithelial cells and the extracellular matrix due to an abnormal PTP zeta/beta signal is the main mechanism of gastric ulceration.