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How Does Helicobacter pylori Cause Mucosal Damage? Its Effect on Acid and Gastrin Physiology

1997; Elsevier BV; Volume: 113; Issue: 6 Linguagem: Inglês

10.1016/s0016-5085(97)80010-8

1528-0012

J Calam, Anita Gibbons, Zoe V. Healey, Philip Bliss, Naila Arebi,

Galectins and Cancer Biology

Helicobacter pylori infection increases gastric acid secretion in patients with duodenal ulcers but diminishes acid output in patients with gastric cancer and their relatives.Investigation of the basic mechanisms may show how H. pylori causes different diseases in different persons.Infection of the gastric antrum increases gastrin release.Certain cytokines released in H. pylori gastritis, such as tumor necrosis factor a and specific products of H. pylori, such as ammonia, release gastrin from G cells and might be responsible.The infection also diminishes mucosal expression of somatostatin.Exposure of canine 0 cells to tumor necrosis factor a in vitro reproduces this effect.These changes in gastrin and somatostatin increase acid secretion and lead to duodenal ulceration.But the acid response depends on the state of the gastric corpus mucosa.The net effect of corpus gastritis is to decrease acid secretion.Specific products of H. pylori inhibit parietal cells.Also, interleukin 113, which is overexpressed in H. pylori gastritis, inhibits both parietal cells and histamine release from enterochromaffinlike cells.H. pylori also promotes gastric atrophy, leading to loss of parietal cells.Factors such as a high-salt diet and a lack of dietary antioxidants, which also increase corpus gastritis and atrophy, may protect against duodenal ulcers by decreasing acid output.However, the resulting increase of intragastric pH may predispose to gastric cancer by allowing other bacteria to persist and produce carcinogens in the stomach. Before Helicobacter pylori was discovered, thoughts on the etiology and treatment of gastroduodenal disorders were dominated by gastric acid.Now it is clear that H. pylori plays a major causative role in gastric and duodenal ulcers (DDs) as well as gastric cancer of the intestinal type.Studies of gastric physiology in patients are revealing complex interactions between the bacterium and gastric acid that seem to predict the clinical outcome.For example, among infected patients, acid secretion tends to be high in patients with DDs but low in those with gastric cancer and their close relatives.Therefore, examining the mechanisms responsible for these various changes in physiology should illuminate the pathways that lead to the different clinical outcomes of this infection.