Campylobacter pyloridis, urease, hydrogen ion back diffusion, and gastric ulcers

Abstract

Campylobacter pyloridis, a bacterium implicated as the aetiological agent of gastritis and possibly gastric ulcers, has a very high urease activity. The rapid hydrolysis of urea at intercellular junctions results in alterations in the milieu of the gastric epithelium preventing the normal passage of hydrogen ions (H+) from the gastric glands through the mucus to the lumen and permits back diffusion. A consequence of H+ back diffusion is hypochlorhydria and a predisposition to ulcer formation. Several conflicting reports on the physiology of normal, gastritis, and ulcerated stomachs are reconciled by this hypothesis.