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Gastric epithelial cell proliferation and apoptosis in Helicobacter pylori‐infected mice
Author(s) -
Yamaguchi T.,
Nakajima N.,
Kuwayama H.,
Ito Y.,
Iwasaki A.,
Arakawa Y.
Publication year - 2000
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.2000.014s1068.x
Subject(s) - helicobacter pylori , apoptosis , medicine , cell growth , spirillaceae , helicobacter infections , gastric mucosa , cancer research , stomach , immunology , gastritis , biology , biochemistry , genetics
Summary Background : Helicobacter pylori causes gastritis and is strongly associated with gastroduodenal ulcer and gastric cancer. The bacterium is associated with an increased rate of epithelial proliferation, which can be reversed by eradication of the organism. The mechanism of this response is not known, but this epithelial proliferation is one of the risk factors for developing gastric carcinoma. Recently, apoptosis also was found to be increased in the gastric mucosa of persons carrying H. pylori . Methods : cagA ‐positive H. pylori isolated from a human gastric ulcer was inoculated into BALB/C mice. At 4, 6, 12, 18 and 24 weeks, mice were injected with bromodeoxyuridine 5 mg/kg and killed 1 h later. Proliferation was analysed by histochemical staining for BrdU; apoptosis was examined by the TUNEL assay. Results : The number of BrdU‐labelled cells in the antrum was significantly increased by H. pylori infection beginning 12 weeks after infection. The number of apoptotic cells in this tissue was increased significantly by 6 weeks after inoculation. Conclusion : The proliferation observed in H. pylori infection may be a response to increased apoptosis.