Systemic cellular immune response in helicobacter pylori associated duodenal ulcer and chronic antral gastritis

Yuceyar H., Saruc M. , Kokuludag A., Terzioglu E., Goksel G., Isisag A.

Turkish Journal of Gastroenterology, vol.11, no.3, pp.208-211, 2000 (Journal Indexed in SCI Expanded) identifier

  • Publication Type: Article / Article
  • Volume: 11 Issue: 3
  • Publication Date: 2000
  • Title of Journal : Turkish Journal of Gastroenterology
  • Page Numbers: pp.208-211


Background/aims: The exact pathogenesis of Helicobacter pylori infection is not fully understood. This study aimed to evaluate the specific subset composition of peripheral blood lymphocytes in patients with Helicobacter pylori positive duodenal ulcer (n = 14) and chronic antral gastritis (n = 28), since reports to date have given inconclusive and conflicting results. Methods: Fourty-two Helicobacter pylori positive patients with duodenal ulcer or chronic antral gastritis and 50 Helicobacter pylori negative control subjects with dyspepsia but without duodenal ulcer or chronic antral gastritis, underwent the following procedures: 1) gastroscopy and gastric biopsy (five specimens) 2) histology, 3) serologic test for anti-Helicobacter pylori antibodies IgG (Pyloriset EIA-G, Orion Diagnostica) and anti-cytotoxin associated gene A (chronic antral gastritis A) IgG antibodies (VIVA Diagnositika by ELISA), 4) analysis of peripheral blood lymphocytes using monoclonal antibodies reacting with lymphocyte cell surface antigens (anti-CD3, anti-CD19, anti-CD4, anti-CD8, anti-CD16 + CD56, anti-HLA DR) by flow-cytometry (Becton-Dickinson). The aim of this was to detect possible changes in lymphocyte subpopulations in patient and control groups. All biopsy samples were studied for Helicobacter pylori density, chronic inflammation, activity, intestinal metaplasia, atrophy and the presence of lymphoid aggregates (according to Sydney system) by histological examination. Patients were considered to have Helicobacter pylori infection if both histology and rapid urease test showed Helicobacter pylori presence. Control subjects were determined by the negativity of both tests at the same time. Results: The control group had a lower degree of chronic inflammation and intestinal metaplasia than the other groups (p<0.05). The percentages of atrophy and lymphoid aggregates present were also significantly lower in the control group than patient groups (p<0.05). Although there was a great difference in the inflammatory response in gastric tissue between the patient and control groups, there was no alteration in total T and B lymphocytes and CD4+T or CD8+T lymphocytes and natural killer (NK) cells between the groups (p>0.05). Although there was a slight increase in the proportion of active T lymphocytes in the patient groups compared to control subjects, this difference was not significant (p>0.05). Conclusions: These data indicate that there is no systemic alteration in the specific immune system in response to Helicobacter pylori in patients with duodenal ulcer and chronic antral gastritis.