Animal Models For H Pylori And Gastric Cancer

Evidence to link H. pylori with gastric cancer has been provided by animal models. In mice, H. hepaticus causes low-grade infection of intrahepatic bile canaliculi; it produces hepatic carcinoma in males of the A/JCr strain (74,75). Liver cells in these animals exhibit both increased cell turnover and increased oxidative damage; they also demonstrate a range of mutations (75-77). This model, however, although useful for the understanding of carcinogenesis, has limited applicability to human gastric cancer.

H. mustelae, a pathogen of ferrets, has many parallels to H. pylori (78). It attaches to the gastric mucosa in a manner similar to H. pylori, and causes chronic inflammation, hypochlorhydria and elevations in serum gastrin levels. Ferrets with H. mustelae frequently develop gastric atrophy (79); gastric adenocarcinoma occurs consistently when infected animals are exposed to the mutagen A-methyl-A-nitro-A'-nitrosoguanidine (MNNG) (80).

Rhesus monkeys can be infected experimentally with H. pylori. As in humans, the infection can be transient or persistent, and may cause both gastritis and an elevated antibody response (81,82). Interplay between characteristics of both the monkey host and the infecting H. pylori strain probably determine the type of gastric response that occurs, as individual monkeys differ in their susceptibility to the infection and the bacterial strains differ in their ability to sustain their presence (83). Because monkeys in colonies tend to become naturally infected, monkey populations provide a useful place for the testing of potential anti-H. pylori therapies and vaccines (84,85).

The most recent model to be identified has been that of the Mongolian gerbil (86). Readily infected with H. pylori, Mongolian gerbils develop gastritis, gastric ulceration, intestinal metaplasia, and gastric adenocarcinoma (87-89). Of note, H. pylori alone appears to be sufficient to cause cancer in this model. While much remains to be discovered, particularly with respect to epithelial alterations, this system should provide a particularly good model for the understanding of the progression from infection to malignancy.

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