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Long-term Evaluation of Mouse Model Infected with Helicobacter pylori and Influence of Helicobacter pylori Infection on Gastric Carcinogenesis

Other Title
장기 Helicobacter pylori 감염 마우스 모델 수립과 위암 발생에 미치는 영향
김, 성우; 차, 충근; 한, 상욱; 김, 영배; 이, 원흥; 주, 희재; 조, 용관; 조, 성원; 김, 명욱; 함, 기백
The Korean journal of gastroenterology, 39(1):22-32, 2002
Journal Title
The Korean journal of gastroenterology; Taehan Sohwagi Hakhoe chi
Background/Aims: This study was aimed to evaluate the long-term outcome of Helicobacter pylori (H. pylori)

infection in mouse model and to know the influence of H. pylori infection on gastric carcinogenesis.

Methods: Four-week-old specific pathogen free C57BL/ 6 mice (n=115) were infected with SS1, the mouse-adapted H. pylori strain. In the 4, 8, 16, 24, 36, 50 and 80 weeks after the bacterial inoculation, the H. pylori-infected mice were sacrificed.

Results: After 80 weeks of infection, most of H. pylori-infected mice developed hyperplastic gastritis, but did

not show any evidence of adenoma, dysplasia or carcinoma. Proliferating cell nuclear antigen-positive cells were most abundant at 50 weeks and tended to decrease at 80 weeks. Apoptosis was noted at 8 weeks after H. pylori infection, showing 7-8 apoptotic cells/high power field and tended to increase with the lapse of time. Normally observed neutral mucin was decreased with the lapse of time and it was remarkably decreased at 50 weeks after H. pylori infection. However, acidic mucin was remarkably noted from 50 weeks after the infection.

Conclusions: SS1-infected mice seem to be suitable for H. pylori-related research and H. pylori itself does not induce gastric cancer in normal wild-type mice model in a long-term study, which could be explained by the balance between cell proliferation and apoptosis.
Helicobacter pyloriC57BL/ 6 miceGastric carcinogenesisApoptosisCell proliferation
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Journal Papers > School of Medicine / Graduate School of Medicine > Gastroenterology
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