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The gene of  Helicobacter pylori  can encode three to four type IV secretory systems, of which a new gene region has been found in the  H. pylori  plasticity region. The coding products of this region can form a new T4SS named tfs3, but its function is unclear. This study investigated the effect of VirD4 recombinant protein in the tfs3 secretory system of the  H. pylori  clinical strain SBK on GES-1 cells. We observed changes in cell morphology after VirD4 treatment. Further analysis indicated that VirD4 increased inflammation by increasing the activation of NF-κB. VirD4 can also inhibited proliferation, and induced migration of cells. Moreover, VirD4 caused apoptosis in GES-1 cells in caspase and ERK1/2/Ras dependent signaling events. Our study laid a foundation for further research on the biological function of VirD4 and the detection and treatment of  H. pylori -related diseases.

Effect of VirD4 on gastric epithelial-1 cells and its mechanism