Production of IL-12 in gastritis relates to infection with Helicobacter pylori

Increased production of proinflammatory cytokines, including tumour necrosi s factor-alpha (TNF-alpha), IL-1 beta, IL-6 and IL-8, has been demonstrated in Helicobacter pylori-associated gastric mucosal inflammation. IL-12, a n ewly characterized cytokine, is thought to be a key mediator in host respon ses to bacterial infections. The aim of this study was to investigate diffe rences in cytokine patterns between H. pylori-positive and -negative gastri tis and normal mucosa. Secretion of IL-12, TNF-alpha, IL-1 beta, IL-6, IL-8 and IL-10 was measured in 176 patients with chronic gastritis in whole bio psy cultures. Gastritis was graded for chronic inflammation or acute inflam matory activity, respectively, according to the Sydney system. Biopsies wit h similar scores were matched for analysis from H. pylori-infected and noni nfected patients. Secretion of IL-12 was significantly increased in H. pylo ri-associated gastritis in comparison with H. pylori-negative gastritis (P < 0.0001). In contrast, secretion of TNF-alpha, IL-1 beta, IL-6, and IL-8 c orrelated with the degree of inflammation but was not different between H. pylori-positive and -negative patients. Moreover, IL-10 secretion was found to be higher in H, pylori-positive than in H. pylori-negative patients. IL -12 may play a specific role in H. pylori-associated gastric disease, where as production of the proinflammatory cytokines TNF-alpha, IL-1 beta, IL-6 a nd IL-8 does not seem to be restricted to H. pylori-induced inflammation. T he contra-inflammatory cytokine IL-10 may be a contributor to the chronicit y of H. pylori-associated gastritis by impairing clearance of the pathogen.