BACKGROUND: The mechanisms by which Helicobacter pylori damages host tissues are complex and unclear. AIMS: To determine the effect interleukin (IL)-4 and interferon-gamma (IFN-gamma) on the production of proinflammatory cytokines by the gastric mononuclear cells of H. pylori infected patients was determined. METHODS: The effect of IL-4 and IFN-gamma on the production of proinflammatory cytokines by the gastric mononuclear cells of H. pylori infected patients was determined. RESULTS: IL-4 markedly reduced the production of IL-1 beta and tumour necrosis factor-a (TNF-alpha) by the gastric mononuclear cells of H. pylori infected patients (P < 0.01). Enzyme-linked immunospot (ELISPOT) assay indicated a decrease in IL-4 producing cells (P < 0.05) and an increase in IFN-gamma secreting cells (P < 0.01). CONCLUSIONS: The increased level of proinflammatory cytokines may be due to hyposecretion of IL-4 in H. pylori infected patients. T helper type 1 (Th1) immune response with increased IFN-gamma also contributes to the inflammation of the gastric mucosa.
BACKGROUND: The mechanisms by which Helicobacter pylori damages host tissues are complex and unclear. AIMS: To determine the effect interleukin (IL)-4 and interferon-gamma (IFN-gamma) on the production of proinflammatory cytokines by the gastric mononuclear cells of H. pylori infectedpatients was determined. METHODS: The effect of IL-4 and IFN-gamma on the production of proinflammatory cytokines by the gastric mononuclear cells of H. pylori infectedpatients was determined. RESULTS: IL-4 markedly reduced the production of IL-1 beta and tumour necrosis factor-a (TNF-alpha) by the gastric mononuclear cells of H. pylori infectedpatients (P < 0.01). Enzyme-linked immunospot (ELISPOT) assay indicated a decrease in IL-4 producing cells (P < 0.05) and an increase in IFN-gamma secreting cells (P < 0.01). CONCLUSIONS: The increased level of proinflammatory cytokines may be due to hyposecretion of IL-4 in H. pylori infectedpatients. T helper type 1 (Th1) immune response with increased IFN-gamma also contributes to the inflammation of the gastric mucosa.