Helicobacter pylori (H.p.) causes active chronic gastritis in nearly all infected patients. Cytotoxic factors elaborated by H.p. as well as autoimmune cell damage from the abundant inflammatory response contribute to gastric epithelial cell injury. Antrum gastritis increases gastrin release. The impact of H.p.-infection on gastric acid physiology is complex and usually results in increased gastric acid secretion in duodenal ulcer patients and diminished acid output in patients with gastric cancer. Multiple clinical outcomes including asymptomatic gastritis, duodenal ulcer, gastric ulcer, gastric carcinoma and gastric MALT lymphoma are associated with H.p.-infection. Differences in disease manifestation seem to result from a complex interaction of bacterial virulence, host factors as well as environmental factors. The acid-secretory ability of the infected individual seems to be the main variable determining outcome: Patients with high acid production typically develop antrum-predominant gastritis and are at an increased risk for duodenal ulcer. In contrast patients with low gastric acid secretion frequently develop pangastritis, which may progress to chronic atrophic gastritis and carcinoma.