The influence of helicobacter pylori colonisation density and the mucosal inflammatory response on gastric acid secretion

Mullins, Paul Dominic (1999) The influence of helicobacter pylori colonisation density and the mucosal inflammatory response on gastric acid secretion. University of Southampton, Doctoral Thesis.

Abstract

The mechanism(s) by which Helicobacter pylori infection alters gastric acid secretion is poorly understood. This thesis describes the history and immunopathology of Helicobacter pylori infection, the control of gastric acid secretion and the relationship between them.

Glycol methacrylate resin immunohistochemistry has been applied to gastric mucosal biopsy tissue in order to accurately quantify mucosal inflammatory cell recruitment. Clinical and histochemical techniques have been used to study the influence of gastric antral and body mucosal Helicobacter pylori colonisation density and inflammatory cell response on fasting and gastrin releasing peptide-stimulated acid secretion and gastric acid secretory capacity in infected chronic duodenal ulcer and non-ulcer dyspeptic subjects.

There are negative correlations between antral Helicobacter pylori colonisation density and fasting acid secretion and gastric acid secretory capacity in active duodenal ulcer disease and non-ulcer dyspepsia but not in those with inactive duodenal ulcer. Thresholds of bacterial load and acid secretory capacity, in combination, are required for active duodenal ulceration. It is hypothesised that an equilibrium is reached between antral Helicobacter pylori colonisation density and gastric acid secretory capacity in active duodenal ulcer disease.

Activity and severity of antral inflammation correlates with gastrin releasing peptide-stimulated acid output in inactive duodenal ulcer disease. The degree of antral inflammation in chronic duodenal ulcer disease increases output with consequent ulcer formation. In Helicobacter pylori-infected non-ulcer dyspeptics increased severity of antral chronic inflammation and activity of inflammatory response in the gastric body is associated with decreased acid secretion which may protect this disease group from duodenal ulcer formation.

Differences in mucosal T lymphocyte population recruitment may provide part of the explanation for differences in behaviour of Helicobacter pylori positive duodenal ulcer and non-ulcer dyspeptic subjects with respect to acid secretion.

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