AI Article Synopsis
- Helicobacter pylori causes chronic type B gastritis and is present in nearly all duodenal ulcer patients.
- The infection triggers increased production of inflammatory cytokines, which play a key role in the development of gastritis and peptic ulcer disease.
- Cytokines can both promote inflammation and help prevent ulcers by stimulating substances that protect the gut, and their effects can influence the overall outcome of the infection.
Article Abstract
Helicobacter pylori is the cause of chronic type B gastritis and occurs in almost all patients with duodenal ulcers. Infection with H. pylori is characterized by an increased production of several inflammatory cytokines. Increasing evidence suggests a central role of these cytokines in the pathogenesis of H. pylori-associated gastritis and peptic ulcer disease. Cytokines may be crucial in the recruitment and activation of inflammatory cells and in stimulation of gastrin release. In addition to their proinflammatory properties, cytokines may also inhibit the ulcer occurrence by stimulation of prostaglandins and somatostatin release and by direct impairment of acid secretion. The balance of these factors may determine the clinical outcome of H. pylori infection.
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| http://dx.doi.org/10.1046/j.1365-2362.1998.00306.x | DOI Listing |
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