Effects of Helicobacter pylori infection on gastric parietal cells and E-cadherin in mongolian gerbils

Atrophic gastritis caused by infection with helicobacter pylori is characterized by parietal cell loss,which is a main risk factor for gastric cancer. parietal cells play a crucial role in the regulation of cell lineage maturation and proliferation in the gastric units. among the classical cadherins,e-cadherin plays an important role not only in epithelial cell-cell connections,but also in the maintenance of epithelial polarity and gastric glandular architecture and regulation of cell proliferation. the aim of this study is to elucidate how parietal cells and e-cadherin are altered in gastritis with helicobacter pylori infection. we studied the effects of helicobacter pylori on gastric mucosal e-cadherin 2 weeks after inoculation and investigated the relationship between parietal cell loss and the amount of e-cadherin on parietal cells in mongolian gerbils. the number of parietal cells and amount of staining of e-cadherin below the isthmus were investigated by immunohistochemistry. it was shown that a reduction in intercellular e-cadherin preceded the disappearance of parietal cells. the gastric glands where parietal cells were lost were replaced by mucus secreting cells without e-cadherin. these results suggest that helicobacter pylori damaged e-cadherin on parietal cells and caused massive parietal cell loss,leading to the deregulation of gastric morphology. © the japanese pharmacological society.