Helicobacter pylori infection and tumour necrosis factor-α increase gastrin release from human gastric antral fragments

OBJECTIVES:To investigate the mechanism of the hypergastrinaemia associated with Helicobacter pylori infection by examining the effect of H. pylori infection and the cytokine tumour necrosis factor-α (TNF-α) on gastrin release from human antral fragments. DESIGN:In-vitro experimental study. METHODS:Human antral biopsy fragments were cultured for 6 h with and without TNFα (20ng/ml) and the gastrin released over the following 2-h stimulation period measured by radioimmunoassay. The integrity of the paracrine feedback loop inhibiting gastrin release was tested by concurrent administration of cholecystokinin (CCK). RESULTS:H. pylori-positive fragments were associated with significantly greater bombesin-stimulated gastrin release (increased by 40%, P