Abstract
Since 1983, information has rapidly accumulated on the proposed role of the bacterial strain now called Campylobacter pylori (formerly C. pyloridis) in causing inflammation and damage to cells of the antrum of the stomach. In that year, Warren and Marshall1 reported the presence of these curved bacteria on the surface of gastric antral epithelium in patients with active chronic gastritis. Later, Marshall et al.2 presented evidence that antral mucosa can be present in the duodenum and that these cells can also be infected by C. pylori. They speculated that gastritis predisposes to gastric ulcers because the damaged cells . . .