| Research Abstract |
We examined mechanisms for development of various neoplastic lesions by H.pylori infection in neonatal thymectomized BALB/c mice. Thymectomy was performed 3 days after birth, and H.pylori was infected orally at 2 months after thymectomy, and following results were obtained :
1. When we infected H.pylori to BALB/c mice, persistent infection did not occur so often, and moreover, we hardly observed mucosal inflammation of the stomach.
2. In contrast, when H.pylori was infected to BALB/c mice thymectomized 3 days after birth, persistent infection developed in all the mice, which was associated with prominent inflammation of the gastric mucosa.
3. In these mice, intestinal metaplasia developed in the antral mucosa at 3 months after the infection.
4.In these thymectomized mice, 10% of them developed gastric adenoma at 6 months after the infection. However, gastric cancer could not be observed even 1 year after the infection.
5. In these thymectomized mice, development of lympho-follicles was obse
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rved 2 months after the infection, and moreover, 70% of them developed gastric MALT lymphoma.
6. In these mice, gastric carcinoid formation was observed at 1 year after the infection in about 30% of all the animals. Serum gastrin concentrations of these mice was 1450 * 96 pg/ml, whchi was significantly higher than that of non-infected mice (116 * 10 pg/ml) and that of the infected mice without carcinoid formation (765 * 56 pg/ ml) (P < 0.01). Moreover, in the infected mice who were treated with a specific gastrin receptor antagonist, AG041R, no carcinoid formation was observed.
7. Gastric MALT lymphoma, gastric adenoma, and gastric carcinoid did not develop concomittantly. Rank orders of the number of H.pylori and serum gastrin level was carcinoid > adenoma > MALT lymphoma, whereas that of gastric acid secretion was MALT lymphoma > adenoma > carcinoid.
8. Host factors such as capacity of acid secretion and hormone secretion, and immunological responses may be important for deciding the occurence of various disease phenotypes. Less
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