Campylobacter pyloridis, urease, hydrogen ion back diffusion, and gastric ulcers.
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.
Hazell
S L
SL
Lee
A
A
D002167:Campylobacter / Q000201:enzymology*; D004058:Diffusion; D005753:Gastric Mucosa / Q000378:metabolism; D005756:Gastritis / Q000150:complications / Q000209:etiology; D006801:Humans; D006863:Hydrogen-Ion Concentration; D011522:Protons; D013276:Stomach Ulcer / Q000209:etiology*; D014508:Urea / Q000378:metabolism; D014510:Urease / Q000378:metabolism*
D011522:Protons; D014508:Urea; D014510:Urease