Mechanism by which Helicobacter pylori infection causes gastric ulcers Mongolian gerbils

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This study was designed to clarify the mechanism of Helicobocter pylori (H.pylori)-induced gastric ulcers in Mongolian gerbils. H.pylori of a VacA- and CagA-positive standard strain (NCTC11637) was once orally inoculated to the animals. H.pylori infection resulted in mucosal inflammation including neutrophil infiltration, associated with cytokine-induced neutrophil chemoattractant (CINC) expression. Thereafter, hemorrhagic lesions occurred in the fundus, followed by generation of ulcers in the same area. Eradication of H.pylori eliminated both CINC expression and gastritis with lesions. Inhibition of acid secretion by omeprazole also improved H.pylori-induced gastric pathology, On the other hand, H.pylori infection impaired mucus synthesis prior to ulceration, and exposure of gastric epithelial cells to H.pylori caused a marked decrease in mucus secretion. Interferon-gamma (IIFNgamma) was induced when gastritis became severe, and exerted a potent inhibitory effect on mucus secretion in the presence of H.pylori. Inhibition of prostaglandin (PG) synthesis by indomethcin accelerated H.pylori-induced gastric ulceration, although the drug did not cause any lesions or ulcers in normal animals. These results suggest that CINC, neutrophil infiltration, gastric acid and IFNgamma serve as deleterious factors in generation of H.pylori-induced gastric ulcers, while gastric mucus and PGs play protective roles in the gastric mucosa.