致命的合作: 幽门螺杆菌与泡菜或熏肉

dr.qinan

By some estimates, more than 50% of the world's population is infected by the bacterium Helicobacter pylori, a gastrointestinal pathogen most famous for its role in the development of gastric ulcers. H. pylori infection is also a risk factor for gastric cancer, but because only a small percentage of infected individuals develop the disease, it would be of great interest to identify controllable lifestyle factors that might contribute to an enhanced risk of cancer. Correlative data from epidemiological studies have suggested a potential interaction between H. pylori infection and diet, but long-term human studies that would establish a cause-effect relationship are not feasible.

In a carefully controlled 5-year study of Rhesus monkeys that were monitored at frequent intervals by gastroscopy and biopsy, Liu et al. found that gastric neoplasia (precancerous and cancerous lesions) developed in H. pylori–infected animals that had also consumed a carcinogen similar to one found in pickled vegetables and smoked meats, but not in animals exposed to either the bacterium or the carcinogen alone. In terms of cancer prevention strategies, these findings underscore the importance of dietary awareness in individuals known to be infected with H. pylori.

http://www.sciencemag.org/content/vol325/issue5945/twil.dtl

原文

Liu H, Merrell DS, Semino-Mora C, Goldman M, Rahman A, Mog S, Dubois A. Diet Synergistically Affects Helicobacter pylori-Induced Gastric Carcinogenesis in Nonhuman Primates.Gastroenterology. 2009 Jul 19. [Epub ahead of print]

ACKGROUND & AIMS: Gastric cancer results from a combination of Helicobacter pylori (H pylori) infection, exposure to dietary carcinogens, and predisposing genetic make-up. Because the role of these factors in gastric carcinogenesis cannot be determined readily in human beings, the present study examined the role of an oral carcinogen and H pylori infection in rhesus monkeys.

METHODS: Gastroscopies were performed in 23 monkeys assigned to 4 groups: controls; nitrosating carcinogen ethyl-nitro-nitrosoguanidine administration alone; and inoculation of a virulent H pylori strain alone (H), or in combination with ethyl-nitro-nitrosoguanidine (EH). Follow-up gastroscopies and biopsies were performed at 3-month intervals for 5 years for pathologic and molecular studies.

RESULTS: Postinoculation, H and EH groups showed persistent infection and antral gastritis. Starting at 2 and 5 years, respectively, gastric intestinal metaplasia and intraepithelial neoplasia developed in 3 EH monkeys but in no other groups. Transcriptional analysis of biopsies at 5 years revealed group-specific expression profiles, with striking changes in EH monkeys, plus a neoplasia-specific expression profile characterized by changes in multiple cancer-associated genes. Importantly, this neoplastic profile was evident in nonneoplastic mucosa, suggesting that the identified genes may represent markers preceding cancer.

CONCLUSIONS: Gastric intraglandular neoplasia is induced in primates when H pylori infection is associated with consumption of a carcinogen similar to the nitrosamines found in pickled vegetables, suggesting that H pylori and the carcinogen synergistically induce gastric neoplasia in primates