| Budget Amount *help |
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥600,000 (Direct Cost: ¥600,000)
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| Research Abstract |
It is now generally accepted that Helicobacter pylori infection is a major cause of chronic gastritis and peptic ulcers. Although epidemiological studies have indicated that H. pylori infection plays a crucial role in gastric carcinogenesis in human, there have been few reports demonstrating a relation between H. pylori and stomach cancer in animal models. In the present study, we first examined the colonizing abilities of eight H. pylori strains in order to select H. pylori strain which could colonize the mouse stomach. Three strains (ATCC43504,CPY2052,and HPK127) colonized C57BL/6 mice, and only CPY2052-infected mice developed a severe gastric inflammation in the lamina propria and erosions in the gastric epithelium 15 months after infection. Secondly, the effect of H. pylori infection on N-methyl-N-nitro-N-nitrosoguanidine (ENNG)-induced gastric cancer was studied using a mouse model. Five-week-old male C57BL/6 mice were divided into four groups of 20-30 animals each and challenged with H. pylori (H. felis), ENNG, a combination of H. pylori (H. felis) and ENNG, or neither of them. Five to 20 animals from each group were sacrificed at 20 and 50 weeks after H. pylori (H. felis) inoculation, and histopathological changes in their stomachs were examined. The incidence of adenomatous hyperplasia in the combination group was significantly higher than that in the ENNG group (p<0.05). These results suggest that H. pylori infection enhances the carcinogenic action of ENNG. This mouse model may be useful for the study of pathogenesis, the screening of novel therapeutic agents, and the development of vaccines.
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