Interferon-gamma and Tumour Necrosis Factor Production in Patients withHelicobacter pylori Infection

Abstract

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.

Expression of CD44 and its variants on gastric epithelial cells of patients with Helicobacter pylori colonisation.

“…Production of TNF-ot and IFN--y was found to be increased in gastric mucosa in H pylorn positive individuals. 32 3 In contrast to HLA class II, we did not find an increase in CD44 expression on gastric IEL. This suggests that other factors in addition to IFN-y (possibly TNF-ot) may be needed for CD44 expression in IEL, and probably also in other cells such as gastric EP.…”

Low pH and Helicobacter pylori increase nuclear factor kappa B binding in gastric epithelial cells: A common pathway for epithelial cell injury?

“…Bacterial strains also appear to be important in eliciting this response as shown by the ability of Cag-specific proteins within the Cag pathogenicity island of H. pylori to enhance NF-kB activation [Glocker et al, 1998]. In addition, H. pylori induces a potent immune response with increased production of the pro-inflammatory cytokines TNF-a and IL-1, both of which directly activate NF-kB [Crabtree et al, 1991;Fan et al, 1993]. Hence NF-kB activation in gastric epithelial cells may result from either direct contact with the bacterium or as a consequence of the immune response to the H. pylori.…”

Biomarkers in Patients with Gastric Inflammation: A Systematic Review

“…On the other hand, Karttunen et al[107] demonstrated an increase in IFN-γ-secreting cells but not in IL-4-secreting cells in both H. pylori -positive and -negative gastric inflammation, suggesting the independence of Th1 type reaction on a pathogenetic or protective role in H. pylori -associated gastric inflammation. In the gastric explant culture from the H. pylori -positive and -negative groups, levels of IFN-γ did not differ significantly [102]. Another study demonstrated that although TNF production by antral mucosa cells in H. pylori- positive patients increased, no significant increase in IFN-γ has been shown.…”

“…Dynamics in IL-4 or IFN-γ in gastritis were also evaluated by 6 citations [69,][71,][81, 102, 106, 107]. Agnihotri et al[106] showed an increase in IL-4 and IL-6 as well as in CD8 + lymphocytes and natural killer cells in H. pylori -associated gastric inflammation.…”

“…In the former studies, most investigations were designed as cross-sectional studies with the exception of 1 case-controlled study, 1 randomized study, and 3 prospective studies. Among 50 selected citations, 32 reports discussed IL-8 as a biomarker for gastric inflammation [65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84,85,86,87,88,89,90,91,92,93,94,95,96], 11 reports described IL-1 as a biomarker for gastric inflammation [66, 69, 77, 82, 92,97,98,99,100,101], and 7 reports focused on TNF-α as a marker for gastric inflammation [71, 77, 81, 82, 90, 91, 102] (fig. 1).…”