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Interferon gamma and interleukin 4 secreting cells in the gastric antrum in Helicobacter pylori positive and negative gastritis.
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Little is known of the function of the T cells in the inflammatory infiltrate in Helicobacter pylori associated gastritis. This study thus measured T cell in vivo activation by enumerating the frequency of interferon gamma (IFN gamma) and interleukin 4 (IL 4) secreting cells isolated from the gastric antral mucosa in patients with or without gastritis and in H pylori positive and negative gastritis. Fifty four samples were examined for cytokine secretion. Four antral biopsy specimens from each patient (n = 51) were taken during diagnostic endoscopy. One was used to estimate histological gastritis and the presence of H pylori, and three of the samples were used to isolate T cells by enzymatic digestion. IFN gamma and IL 4 secreting cells were enumerated by ELISPOT. Thirty four samples had gastritis and 79% of those were H pylori positive. None of the samples from non-inflamed mucosa had H pylori. The numbers of IFN gamma secreting cells per 10(5) T cells were higher in gastritis than in normal mucosa (145 v 20 IFN gamma spots, p < 0.01), and higher in H pylori negative than H pylori positive gastritis (371 v 110 IFN gamma spots, p < 0.05). The frequencies of IL 4 secreting cells did not differ between gastritis and non-inflamed mucosa. In conclusion, there is an increase in IFN gamma secreting cells but not in IL 4 secreting cells in H pylori positive and negative gastritis. It is not known if this TH1 type reaction has a pathogenetic or protective role.
Title: Interferon gamma and interleukin 4 secreting cells in the gastric antrum in Helicobacter pylori positive and negative gastritis.
Description:
Little is known of the function of the T cells in the inflammatory infiltrate in Helicobacter pylori associated gastritis.
This study thus measured T cell in vivo activation by enumerating the frequency of interferon gamma (IFN gamma) and interleukin 4 (IL 4) secreting cells isolated from the gastric antral mucosa in patients with or without gastritis and in H pylori positive and negative gastritis.
Fifty four samples were examined for cytokine secretion.
Four antral biopsy specimens from each patient (n = 51) were taken during diagnostic endoscopy.
One was used to estimate histological gastritis and the presence of H pylori, and three of the samples were used to isolate T cells by enzymatic digestion.
IFN gamma and IL 4 secreting cells were enumerated by ELISPOT.
Thirty four samples had gastritis and 79% of those were H pylori positive.
None of the samples from non-inflamed mucosa had H pylori.
The numbers of IFN gamma secreting cells per 10(5) T cells were higher in gastritis than in normal mucosa (145 v 20 IFN gamma spots, p < 0.
01), and higher in H pylori negative than H pylori positive gastritis (371 v 110 IFN gamma spots, p < 0.
05).
The frequencies of IL 4 secreting cells did not differ between gastritis and non-inflamed mucosa.
In conclusion, there is an increase in IFN gamma secreting cells but not in IL 4 secreting cells in H pylori positive and negative gastritis.
It is not known if this TH1 type reaction has a pathogenetic or protective role.
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