Helicobacter pylori(H. pylori) is an important pathogenic factor for gastroduodenal ulcers and gastric cancer. The level of gastric acid output may influence the outcome of those diseases. With low acid output, H. pylori can spread to the corpus of the stomach, resulting in progression to atrophic gastritis. It may cause an increased risk of gastric cancer and ulcer. In contrast, with high output, H. pylori is confined in the gastric antrum, which develops antrum-predominant gastritis. This may contribute to an increased risk of duodenal ulcer. It is well known that inflammatory cytokines including interleukin (IL)-1 beta, IL-8 and tumor necrosis factor alpha modulate gastric acid secretion. Therefore, the host immune response by the cytokines may cause these disparate pathways in gastric acid secretion.