title: [Helicobacter pylori-related cytokines influence gastric acid secretion and gastric mucosal inflammation in gastroduodenal ulcers].
abstract: 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.
authors.affiliation: Division of Gastroenterology, Tohoku University Graduate School of Medicine.
authors.forename: Akira
authors.initials: A
authors.lastname: Imatani
authors.forename: Shuichi
authors.initials: S
authors.lastname: Ohara
authors.forename: Makoto
authors.initials: M
authors.lastname: Yonechi
authors.forename: Motoki
authors.initials: M
authors.lastname: Ohyauchi
authors.forename: Tooru
authors.initials: T
authors.lastname: Shimosegawa
mesh_terms: D005744:Gastric Acid / Q000378:metabolism*; D005757:Gastritis, Atrophic / Q000209:etiology*; D016481:Helicobacter Infections / Q000503:physiopathology*; D016480:Helicobacter pylori; D006801:Humans; D007375:Interleukin-1 / Q000502:physiology*; D016209:Interleukin-8 / Q000502:physiology*; D010437:Peptic Ulcer / Q000209:etiology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
chemical_list: D007375:Interleukin-1; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha