Korean J Gastroenterol.  2002 Jan;39(1):22-32.

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

• Kim SW
• Cha CK
• Han SU
• Kim YB
• Lee WH
• Joo HJ
• Cho YK
• Cho SW
• Kim MW
• Hahm KB

Abstract

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.

Keyword

Helicobacter pylori; C57BL/6 mice; Gastric carcinogenesis; Apoptosis; Cell proliferation

MeSH Terms

Adenoma
Animals
Apoptosis
Carcinogenesis*
Cell Proliferation
Gastritis
Helicobacter pylori*
Helicobacter*
Mice*
Mucins
Specific Pathogen-Free Organisms
Stomach Neoplasms
Mucins