There is a growing body of evidence suggesting that Helicobacter pylori plays a pathogenic role in gastric and duodenal ulceration. A strong association between infection with this organism and the presence of active chronic gastritis in the antrum has been documented. However, the mechanism through which this gastritis and the associated degenerative changes in the mucosa are produced is not fully understood. It is possible that the bacterium itself produces chemotactic factors that recruit granulocytes into the mucosa, although there is scant evidence to indicate the importance of any one mediator over others. Several inflammatory mediators have potent vascular effects, which could predispose the mucosa, in a region of infection, to ulceration. One such mediator, platelet-activating factor, is produced by H. pylori. Further characterization of the mechanism through which H. pylori contributes to the development of gastritis and the inflammatory mediators involved will be facilitated by the development of relevant animal models.