Ｈ．ｐｙｌｏｒｉ感染スナネズミ実験胃癌の抑制

Abstract

Helicobacter pylori (Hp) has been classified as a stomach carcinogen on the basis of epidemiological findings. For detailed analysis of the role of Hp in stomach carcinogenesis, it is essential to establish a small animal model. Hirayama et al. first demonstrated that Mongolian gerbils (MGs) can be infected with Hp. We have established experimental models of stomach carcinogenesis in MGs using the chemical carcinogens, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and N-methyl-N-nitrosourea (MNU). In the present study, male MGs were infected with Hp before or after MNU administration. Glandular stomach adenocarcinomas not only of well-differentiated but also poorly differentiated and signet-ring cell types were induced. The incidence of adenocarcinomas was significantly higher in animals treated with before or after MNU administration than in the controls. Hp infection also enhances glandular stomach carcinogenesis in MGs treated with MNNG. To further assess this latter possibility, male MGs were treated with MNU followed by inoculation with Hp, or infected with Hp followed by MNU administration, then Hp was eradicated in half of the infected animals. The incidence of tumor development in infected animals was significantly higher than in Hp eradicated animals. The incidence was significantly suppressed by the eradication procedure. Our studies have shown that Hp enhances glandular stomach carcinogenesis of MGs treated with chemical carcinogens. Moreover, Hp eradication may be useful as a prevention approach.