Diminished interferon-gamma production in gastric mucosa T lymphocytes after H. pylori eradication in duodenal ulcer patients.
OBJECTIVE
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.


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 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.
Ihan
A
A
Institute of Microbiology, Medical Faculty, Ljubljana, Slovenia. IHAN@.MF.UNI-LJ.SI
Tepez
B
B
Gubina
M
M
Malovrh
T
T
Kopitar
A
A
D000658:Amoxicillin / Q000009:adverse effects / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000009:adverse effects / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D004381:Duodenal Ulcer / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D005434:Flow Cytometry; D005500:Follow-Up Studies; D005753:Gastric Mucosa / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D016480:Helicobacter pylori / Q000187:drug effects* / Q000276:immunology; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism*; D015847:Interleukin-4 / Q000032:analysis; D008795:Metronidazole / Q000009:adverse effects / Q000627:therapeutic use; D009942:Organometallic Compounds / Q000009:adverse effects / Q000627:therapeutic use; D015375:Receptors, Interleukin-2 / Q000032:analysis / Q000187:drug effects; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D016896:Treatment Outcome
D000900:Anti-Bacterial Agents; D009942:Organometallic Compounds; D015375:Receptors, Interleukin-2; D008795:Metronidazole; D015847:Interleukin-4; D000658:Amoxicillin; D007371:Interferon-gamma; C002791:bismuth tripotassium dicitrate