An Animal Model of Gastritis Induced by Campylobacter pylori

Abstract

Following confirmation of the findings [1, 5, 10–12] first reported by Warren and Marshall [13] that gastritis and peptic ulcers are frequently associated with Campylobacter pylori colonization of gastric and duodenal mucosae, the major unresolved question concerns the role of the bacterium in these disease states. Unknown is whether C. pylori causes the inflammation and ulceration or simply secondarily colonizes the diseased tissue. Evidence is accumulating which suggests that the bacterium is a pathogen. We have previously reported that C. pylori produces a toxic factor that induces intracellular vacuolization in cultured mammalian cells. Similar intracellular vacuolization has been observed in tissues from patients suffering chronic gastritis [11]. Marshall [8] and Morris [9] have described their personal experiences on the development of gastritis following ingestion of the organism.