(J7 Clin Pathol 1995;48:133-136)

Helicobacter pylori has been identified as a dominant factor in the pathogenesis of duodenal ulcer. The aim of this study was to examine peripheral blood and gastric lymphocyte proliferation and cytokine production in patients with H pyloni colonisation. Sixty five dyspeptic patients attending for endoscopy were studied; 35 of these were H pyloni positive

The direct and indirect effects of Helicobacter pylori on cell kinetics of gastric epithelial cell line AGS were investigated by flow cytometric analysis of

Background-Studies have suggested that expression of the adhesion molecule CD44 may be of prognostic importance in gastric cancer. In addition, there is strong

The production of the cytokines, interferon-gamma and tumour necrosis factor by human antral mucosa cells and stimulated peripheral blood mononuclear cells were determined by enzyme linked immunosorbent assay and L929 bioassay respectively. Tumour necrosis factor production by peripheral blood mononuclear cells in response to Helicobacter pylori stimulation was depressed in Helicobacter pylori positive individuals, compared to Helicobacter pylori negative individuals (P < 0.05). There was no difference in tumour necrosis factor production by peripheral blood mononuclear cells in response to purified protein derivative. However, tumour necrosis factor production by cells isolated from gastric mucosa during short term culture was significantly higher in Helicobacter pylori positive patients (P < 0.05) than negative patients, indicating a probable macrophage response. Levels of interferon-gamma did not differ significantly in the gastric explant culture from the two groups. The results show that Helicobacter pylori negative patients have a stronger peripheral cellular immune response to Helicobacter pylori infection. The higher levels of tumour necrosis factor production by antral mucosa cells in Helicobacter pylori positive patients may reflect the infiltration of T lymphocytes and macrophages within the local mucosa.

Several lines of evidence implicate Helicobacter pylori (H. pylori) infection in gastroduodenal inflammation. However, the exact pathogenesis of H. pylori infection is not fully understood. T-helper (TH) lymphocytes may be subdivided into TH1 and TH2 cells based on the distinct patterns of cytokine production. TH1 reaction is associated with immunity or resistance to infection, while TH2 reaction is associated with the progression or persistence of infection. The production of interferon-gamma (INF-gamma) and interleukin 2 (IL-2), which are type 1 cytokines, is decreased in H. pylori infection. Enhanced production of type 2 cytokines (IL-4) and IL-6) is observed in individuals with H. pylori infection. Suppressed proliferative responses of peripheral blood and gastric lymphocytes have also been demonstrated in patients with H. pylori colonisation, suggesting that specific T-cell responses may be down-regulated by an enhanced TH2 reaction. Suppressed TH1 and enhanced TH2 responses in H. pylori infection may be involved in the immunopathogenesis of chronic H. pylori infection.

Hellcobacter pylori is the most common cause of gastroduodenal inflammation. However, the exact immune pathogenesis is not fully understood. To look for evidence of the immunological mechanism in H. pylori associated disease, we measured cytokine interleukin-2 (IL-2) and IL-4 levels produced by peripheral blood lymphocytes (PBL) and gastric biopsies in 20 subjects with or without H. pylori infection. H. pylori can stimulate IL-2 and IL-4 production from PBL in H. pylori negative as well as H. pylori positive individuals. The spontaneous IL-2 production by PBL and gastric biopsies was greater (p < 0.0025, <0.001)in H. pylori negative individuals than that in H. pylori infected patients. Increased IL-4 levels from PBL in H. pylori infected patients were found in the presence of H. pylori (p < 0.0025). An increased spontaneous production of IL-4 from gastric biopsies was also observed in H. pylori infected patients (p < 0.025). In conclusion, an enhanced type 2 cytokine production was observed in H. pylori infected patients, which may be responsible for H. pylori chronic infection.

No abstract