| First Author | Kim DH | Year | 2003 |
| Journal | Aliment Pharmacol Ther | Volume | 18 Suppl 1 |
| Pages | 14-23 | PubMed ID | 12925137 |
| Mgi Jnum | J:85691 | Mgi Id | MGI:2675950 |
| Doi | 10.1046/j.1365-2036.18.s1.4.x | Citation | Kim DH, et al. (2003) Long-term evaluation of mice model infected with Helicobacter pylori: focus on gastric pathology including gastric cancer. Aliment Pharmacol Ther 18 Suppl 1:14-23 |
| abstractText | BACKGROUND: Long-term evaluation of gastric pathology after H. pylori infection is very important in order to reveal its clinical implications, since debate still exists on the gastric carcinogenesis provoked by H. pylori infection in animal models. AIM: Either to evaluate the long-term outcome of H. pylori infection or to determine how H. pylori could provoke gastric cancer in the mice model. METHODS: Four-week-old specific pathogen free C57BL/6 mice (n = 115) were infected with SS1, the mouse-adapted H. pylori strain. After 4, 8, 16, 24, 36, 50 and 80 weeks of bacterial infection, the H. pylori-infected mice were sacrificed. RESULTS: After 80 weeks of infection, almost all the H. pylori-infected mice developed hyperplastic gastritis, but did not show any evidence of gastric adenoma, dysplasia or carcinoma. PCNA positive cells were most abundant after 50 weeks and tended to decrease thereafter up to 80 weeks, whereas apoptosis began to be noted 8 weeks after H. pylori infection, showing 7-8 apoptotic cells/high power field, and tending to increase as time passed. Normally observed neutral mucin decreased during the experiment, showing the most marked decrease 50 weeks after H. pylori infection. In contrast, acidic mucin was noted from 50 weeks after infection. CONCLUSION: The SS1-infected mouse seems to be a suitable animal model for H. pylori-related research, and H. pylori itself does not induce gastric cancer in normal wild-type mouse model following long-term exposure, which could be explained by the balance that exists between cell proliferation and apoptosis. |
