Effect of immunization on gastrin release in rat antrum mucosa.

Helicobacter pylori (H.P.) infection is the main cause of chronic active gastritis and is closely associated with peptic ulcer disease. Chronic hypergastrinaemia is known to be induced in patients infected with this pathogen. Gastrin is the most potent stimulator of gastric acid secretion. In animals infected with H.P. or H. felis vaccination against H.P.can eliminate the bacterium and alleviate associated gastritis. However little is known on the influence of immunization regimes on gastrin release. The aim of this study was to evaluate the effect of systemic immunization on gastrin release in a rat model, using a well defined but for the rat unknown protein. OVA-immunized and non immunized animals received OVA intragastrically in vivo, and serum gastrin was measured. Stimulation with bovine serum albumin (BSA) served as control. In vitro single cell suspensions of the antrum mucosa and mucosal fragments of immunized and non immunized animals were also incubated with OVA and BSA. The results show specific significant gastrin suppression after immunization and antigen feeding. The same results were obtained in the model of mucosa fragments but not in single cell suspensions. This hypothesized that gastric suppression could be mediated by mast cells or T-helper two cells (TH2) in the mucosal layer of the stomach. A single cell suspension is not suitable for studying immunologically mediated gastrin release because direct cell contact is necessary. Further studies with these animal models have to show whether effects seen by vaccination could be mediated by induction of gastrin suppression and studies on human tissues are necessary to show possible similar effects with H.P.