HYPOTHESES ON THE ROLE OF CYTOKINES IN PEPTIC-ULCER DISEASE

Helicobacter pylori is the cause of chronic type B gastritis and occur s in almost all patients with duodenal ulcers. Infection with H. pylor i is characterized by an increased production of several inflammatory cytokines. Increasing evidence suggests a central role of these cytoki nes in the pathogenesis of H. pylori-associated gastritis and peptic u lcer disease. Cytokines may be crucial in the recruitment and activati on of inflammatory cells and in stimulation of gastrin release. In add ition 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 th ese factors may determine the clinical outcome of H. pylori infection.