Background-Interleukin-10 (IL-10) is an 18 kDa peptide with a range of antiinflammatory and immunosuppressive properties. Aim-To determine whether this cytokine is involved in gastric mucosal inflammation in Helicobacterpylori infection.Methods-The production of IL-10 by antral mucosal biopsy specimens during short term in vitro culture was determined by measuring IL-10 content of supernatants by enzyme linked immunosorbant assay (ELISA). H pyloon status was determined by serology and histology, with gastritis scored using the Sydney system. Tumour necrosis factor-a (TNF-ae) content of supernatants was also determined in a subgroup ofpatients. Results-IL-10 secretion was significantly greater in patients with H pylon associated chronic gastritis than in patients who were H pylori negative with normal mucosa/reactive changes, and those with Hpylori negative chronic gastritis (p<001 and <0.05 respectively). There was a significant correlation overall between IL-10 secretion and chronic inflammation score (r=0.40). Secretion of TNF-a, which was significantly higher in H pylon infected patients than uninfected patients with a normal mucosa (p<0.04), correlated with scores for chronic inflammation and activity (r=0.39 and 0-38 respectively), but was only weakly correlated with IL-10 secretion (r=0.22, NS). Conclusions-Gastric mucosal production of IL-10 and TNF-ct are increased in chronic gastritis associated with H pylon infection, and mucosal cytokine secretion varies with important histopathological aspects of gastric inflammation. Whereas the secretion of IL-10 in Hpylon infection may be protective, limiting tissue damage caused by inflammation, it may also contribute towards failure of the immune response to eliminate the organism. (Gut 1997; 40: 739-744) Keywords: interleukin-10, Helicobacterpylori, tumour necrosis factor--a.Histologically, chronic gastritis associated with Helicobacter pylori is characterised by infiltration of the lamina propria by chronic inflammatory cells, the presence of lymphoid follicles, and a variable degree of polymorph infiltration indicative of active inflammation.' The presence of this inflammatory infiltrate suggests a specific immune response directed against the organism. Local cellular immunity, as judged by cytokine production, seems to be activated, with in vitro biopsy studies showing raised mucosal production of proinflammatory cytokines, such as interleukin (IL)-1, IL-6, and IL-8, tumour necrosis factor-a (TNF-a), and interferon--y (IFN-y) in subjects with H pylon associated gastritis.`25 Short term biopsy cultures have also confirmed a local humoral response in infected patients, with in vitro mucosal production of H pylori specific immunoglobulins.6 Despite this evidence for an intact mucosal immune response to Hpylori infection, most people fail to eliminate the organism spontaneously, with infection persisting long term. Although there are probably many factors which contribute to the chronicity of infection, immune suppression or down regulation of local i...
