ABSTRACT
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.
Subject(s)
Anti-Bacterial Agents/therapeutic use , Duodenal Ulcer/drug therapy , Gastric Mucosa/drug effects , Helicobacter Infections/drug therapy , Helicobacter pylori/drug effects , Interferon-gamma/metabolism , Amoxicillin/adverse effects , Amoxicillin/therapeutic use , Anti-Bacterial Agents/adverse effects , Drug Therapy, Combination , Duodenal Ulcer/immunology , Duodenal Ulcer/pathology , Flow Cytometry , Follow-Up Studies , Gastric Mucosa/immunology , Gastric Mucosa/pathology , Helicobacter Infections/immunology , Helicobacter Infections/pathology , Helicobacter pylori/immunology , Humans , Interleukin-4/analysis , Metronidazole/adverse effects , Metronidazole/therapeutic use , Organometallic Compounds/adverse effects , Organometallic Compounds/therapeutic use , Receptors, Interleukin-2/analysis , Receptors, Interleukin-2/drug effects , T-Lymphocytes/drug effects , T-Lymphocytes/immunology , T-Lymphocytes/pathology , Treatment OutcomeABSTRACT
BACKGROUND/AIMS: Helicobacter 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. This study examined the expression of IL-2 receptor and ICAM-1 molecules on gastric mucosa infiltrating T lymphocytes in two groups of H. pylori infected patients: one group with an active ulcer disease and the other with non-ulcerative chronic gastritis. MATERIAL AND METHODS: 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 3-color flow cytometry analysis for the IL-2 receptor (CD25) and ICAM-1 molecule (CD54) expression. Lymphocytes from 37 Helicobacter pylori infected patients with severe gastric mucosa infiltration (G2 and G3 histological type in Sydney classification) were analyzed; 18 patients had at least 5-year history of duodenal ulcer disease (group A) and 19 patients had at least 3-year history of non-ulcer dyspeptic disease (group B). RESULTS: We demonstrated a significant increase in IL-2 receptor expression on gastric mucosa T cells in ulcer patients (group A) compared with non-ulcer dyspeptic patients (group B). However, no difference in CD54 expression was found between the two groups of patients. CONCLUSIONS: Our results suggest the importance of the local immune response in the development of H. pylori related diseases. Also some interesting points for further study of the association between immune response against H. pylori and the development of duodenal ulcer disease were indicated.
Subject(s)
Duodenal Ulcer/metabolism , Gastric Mucosa/metabolism , Gastritis/metabolism , Helicobacter Infections/metabolism , Receptors, Interleukin-2/metabolism , T-Lymphocytes/metabolism , Adult , Aged , Duodenal Ulcer/immunology , Duodenal Ulcer/microbiology , Duodenal Ulcer/pathology , Female , Flow Cytometry , Gastric Mucosa/cytology , Gastric Mucosa/immunology , Gastric Mucosa/pathology , Gastritis/immunology , Gastritis/microbiology , Gastritis/pathology , Helicobacter Infections/immunology , Helicobacter pylori , Humans , Immunophenotyping , Intercellular Adhesion Molecule-1/metabolism , Male , Middle AgedABSTRACT
We isolated lymphocytes from chronically inflamed gastric mucosa. We analysed the expression of IL-2 receptors (CD25), transferin receptors (CD71) and HLA-DR molecules on T lymphocytes by flow cytometric analysis in 16 patients with urease-positive and in 7 patients with urease-negative chronic gastritis. In G0, G1 and G2 histological type (Sydney classification) of gastritis the number of lymphocytes obtained from the gastric mucosa biopsies was too low for the flow cytometric analysis. However, in G3 histological type of chronic gastritis we obtained enough cells for the flow cytometric analysis in 75%. We demonstrated a significant increase in HLA-DR expression on CD8 cells from patients with urease-positive gastritis compared to urease-negative gastritis. We also observed a statistically non-significant increase in HLA-DR expression on CD3 cells, and in CD71 expression on both CD3 and CD8 cells in urease-positive gastritis. However, no difference in CD25 expression was found between the two types of gastritis.
