Histochemical Study of Helicobacter pylori and Surface Mucous Gel Layer in Various Gastric Lesions.

  • Akamatsu Taiji
    The 2nd Department of Internal Medicine, Shinshu University School of Medicine
  • Ota Hiroyoshi
    Department of Laboratory Medicine, Shinshu University School of Medicine
  • Shimizu Toshiki
    The 2nd Department of Internal Medicine, Shinshu University School of Medicine
  • Matsuzawa Kenji
    The 2nd Department of Internal Medicine, Shinshu University School of Medicine
  • Fujimori Yoshifumi
    The 2nd Department of Internal Medicine, Shinshu University School of Medicine
  • Nakamura Naoshi
    The 2nd Department of Internal Medicine, Shinshu University School of Medicine
  • Kiyosawa Kendo
    The 2nd Department of Internal Medicine, Shinshu University School of Medicine
  • Katsuyama Tsutomu
    Department of Laboratory Medicine, Shinshu University School of Medicine

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To elucidate the relation between Helicobacter pylori (H. pylori) and the surface mucous gel layer (SMGL), 32 cases (25 cases of gastric cancer and 7 of peptic ulcer) of surgically removed human stomach were examined by employing histochemical staining for mucins and H. pylori. This organism was demonstrated in 19 cases by histopathological and histochemical observation. All materials were fixed 2hr in cold Carnoy's solution to fix the SMGL and were embedded in paraffin. Serial paraffin sections were stained with galactose oxidase-cold thionin Schiff-paradoxical Concanavalin A staining (GOCTS-PCS). In addition, immunostaining with anti-H. pylori antibody was performed after the GOCTS-PCS sequence. H. pylori was observed not only on the apical surface of the surface mucous cells or between two lateral plasma membranes of adjacent surface mucous cells, but more abundantly in the SMGL. This organism was not found on the metaplastic cells showing intestinal properties, regenerated immature cells surrounding ulcerated lesions and neoplastic epithelial cells of carcinoma. In the SMGL, it tended to distribute in the layers of the surface mucous cell-type mucin, and, when it existed, marked disintegration of mucous layers and vacuolation was evident. These data suggest that disintegration of mucous in the SMGL is one of the factors which accelerate mucosal damage by this agent.

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