Chronic active type B gastritis is invariably the result of Helicobacter pylori infection and is an important factor in duodenal ulcer disease. The actions of mediators produced (a protein factor, a lipid soluble "pore-forming factor" and urease) or induced (immune/inflammatory cell mediators) by this bacterium on the control of gastric acid secretion are currently being investigated. These studies are reviewed in light of our current knowledge of the physiological control of gastric acid secretion.