title: Local cytokine response in Helicobacter pylori-infected subjects.
abstract: The host immune response to Helicobacter pylori infection might be of importance with regard to the outcome of infection by this organism, e.g., to explain why only a proportion of infected subjects develop peptic ulcers. In this study we have analyzed the local response of different cytokines-i.e., the proinflammatory interleukin-1beta, (IL-1beta), IL-6, tumor necrosis factor alpha, and IL-8; the immunoregulatory gamma interferon (IFN-gamma); and IL-4; and the anti-inflammatory transforming growth factor beta (TGF-beta)-in antral biopsy specimens from H. pylori-infected duodenal ulcer (DU) patients and asymptomatic (AS) carriers (i.e., with chronic gastritis only). For comparison, biopsy specimens from uninfected healthy individuals were also analyzed. An immunohistochemical technique was used to allow quantification of the cytokine responses as well as identification of the cell types associated with the cytokine expression. We found that the levels of all of the studied cytokines except IL-4 were increased in the H. pylori-infected subjects compared to the levels in the healthy individuals. Our results indicate that the antral cytokine response is of the Th1 type since IFN-gamma, but not IL-4, was up-regulated both in H. pylori-infected DU patients and in AS carriers. However, there were no significant differences in either proinflammatory or immunoregulatory cytokine levels when H. pylori-infected subjects with and without peptic ulcers were compared. Some of the cytokines, particularly IL-1beta and TGF-beta, were also found in the gastric mucosae of healthy, uninfected subjects. We also showed that the gastric epithelium contributes substantially to the antral cytokine response of the proinflammatory cytokines IL-1beta and IL-6 in addition to IL-8.
authors.affiliation: Department of Medical Microbiology and Immunology, Göteborg University, Göteborg, Sweden. catharina.lindholm@microbio.gu.se
authors.forename: C
authors.initials: C
authors.lastname: Lindholm
authors.forename: M
authors.initials: M
authors.lastname: Quiding-Järbrink
authors.forename: H
authors.initials: H
authors.lastname: Lönroth
authors.forename: A
authors.initials: A
authors.lastname: Hamlet
authors.forename: A M
authors.initials: AM
authors.lastname: Svennerholm
mesh_terms: D000328:Adult; D000368:Aged; D002908:Chronic Disease; D016207:Cytokines / Q000096:biosynthesis*; D004381:Duodenal Ulcer / Q000276:immunology*; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology; D005756:Gastritis / Q000276:immunology*; D016481:Helicobacter Infections / Q000276:immunology*; D016480:Helicobacter pylori; D006801:Humans; D007371:Interferon-gamma / Q000302:isolation & purification; D007378:Interleukins / Q000302:isolation & purification; D007413:Intestinal Mucosa / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011706:Pyloric Antrum / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000302:isolation & purification; D014409:Tumor Necrosis Factor-alpha / Q000302:isolation & purification
chemical_list: D016207:Cytokines; D007378:Interleukins; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma