analyzed the direct effect of H. pylori
OMVs on cellular events associated with carcinogenesis.
They found that the treatment of H. pylori OMVs (from
toxigenic strain 60190) with AGS human gastric epithelial
cells increased the micronuclei formation, while the OMVs
purified from the deletion mutant vacA-did not. They concluded
that OMVs delivery the vacuolating toxin VacA to
the gastric epithelium that may represent a new mechanism
for H. pylori to induce gastric carcinogenesis