Functional Role of Metaplastic Paneth Cell Defensins in Helicobacter pylori-Infected Stomach |
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Authors: | Hiroki Tanabe Tomonobu Sato Jiro Watari Atsuo Maemoto Mikihiko Fijiya Toru Kono Toshifumi Ashida Tokiyoshi Ayabe Yutaka Kohgo |
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Institution: | Division of Gastroenterology and Haematology/Oncology, Department of Internal Medicine, Asahikawa Medical College, Midorigaoka Higashi 2-1-1-1, Asahikawa, Hokkaido 078-8510, Japan,;Division of Surgical gastroenterology, Department of Surgery, Asahikawa Medical College, Midorigaoka Higashi 2-1-1-1, Asahikawa, Hokkaido 078-8510, Japan,;Innate Immunity Laboratory, Faculty of Advanced Life Science, Hokkaido University Graduate School of Life Science, Kita-21 Nishi-11, Kitaku, Sapporo, Hokkaido 001-0021, Japan |
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Abstract: | Background and Aims: Chronic gastritis is caused by Helicobacter pylori infection, and gastritis is classified as inflammation, atrophy, and intestinal metaplasia. Detailed pathologic studies have shown that H. pylori settles on the surface of gastric mucosa, and that it is eliminated from metaplastic mucosa. However, its mechanism of natural protection is not well known. Methods: Antimicrobial human enteric defensin expression was determined in the RNA and protein levels. Recombinant enteric defensins were produced with a bacterial expression system and their anti- H. pylori activities were assessed by bactericidal assay. Results: Human enteric defensin (HD)-5 and HD-6 were detected in Paneth cells, which are observed in the gastric metaplastic mucosa as well as small intestinal epithelia. HD-5 protein was coexpressed with trypsin, which is considered to be an activating enzyme of HD-5. Less H. pylori was observed in the intestinal metaplasia with HD-5 expressing Paneth cells. The recombinant defensins showed killing activity against H. pylori at a low concentration in vitro. Conclusions: The human defensins that are expressed in the metaplastic Paneth cells eliminate H. pylori . Metaplastic change may be a purposive development of the human stomach. |
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Keywords: | Immune response intestinal metaplasia Paneth cells alpha-defensin innate immunity |
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