Background/aims: Helicobacter pylori (H. pylori) infects an estimated 50% of the world population; however, only a small proportion of individuals develop clinical symptoms of gastritis, peptic ulceration or gastric cancer. The variations in disease presentation may be due to differences in bacterial virulence and/or immune response to the pathogen. In a previous study we reported an increased expression of the IL-2 receptor in duodenal ulcer (DU) patients. The present study examines the expression of IL-2 receptor and intracellular lymphokine production in gastric mucosa infiltrating T lymphocytes in DU patients before and after H. pylori eradication.
Methodology: T lymphocytes were isolated from gastric mucosa biopsies by using mechanical and enzymatic tissue desegregation. Ficoll-purified lymphocytes were incubated with monoclonal antibodies and analyzed by using 4-color flow cytometry analysis for the IL-2 receptor (CD25) and intracellular interferon-gamma (IFN-gamma) and IL-4 expression. Lymphocytes from 24 H. pylori-infected patients with severe gastric mucosa infiltration (G2 and G3 histological type in Sydney classification) were analyzed.
Results: We demonstrated a significant decrease in IL-2 receptor expression on gastric mucosa T cells 3 and 12 months after eradication of H. pylori. We also demonstrated a diminished IFN-gamma production 3 and 12 months after H. pylori eradication.
Conclusions: Our results suggest that cellular immune activation in gastric mucosa is reversibly dependent on the presence of H. pylori.