Effects of Helicobacter pylori Infection on Gastric Parietal Cells and E-cadherin in Mongolian Gerbils

  • Murakami Motonobu
    Department of Pharmacotherapy, Faculty of Pharmaceutical Sciences, Doshisha Women’s College of Liberal Arts, Japan
  • Fukuzawa Mayu
    Department of Pharmacotherapy, Faculty of Pharmaceutical Sciences, Doshisha Women’s College of Liberal Arts, Japan
  • Yamamoto Mika
    Department of Pharmacotherapy, Faculty of Pharmaceutical Sciences, Doshisha Women’s College of Liberal Arts, Japan
  • Hamaya Kanako
    Department of Pharmacotherapy, Faculty of Pharmaceutical Sciences, Doshisha Women’s College of Liberal Arts, Japan
  • Tamura Yuumi
    Department of Pharmacotherapy, Faculty of Pharmaceutical Sciences, Doshisha Women’s College of Liberal Arts, Japan
  • Sugiyama Akiko
    Department of Pharmacotherapy, Faculty of Pharmaceutical Sciences, Doshisha Women’s College of Liberal Arts, Japan
  • Takahashi Rei
    Department of Pharmacotherapy, Faculty of Pharmaceutical Sciences, Doshisha Women’s College of Liberal Arts, Japan
  • Murakami Toshiko
    Department of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University, Japan
  • Amagase Kikuko
    Department of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University, Japan
  • Takeuchi Koji
    Department of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University, Japan

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タイトル別名
  • Effects of <i>Helicobacter pylori</i> Infection on Gastric Parietal Cells and E-cadherin in Mongolian Gerbils

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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.

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