Attenuation of Hydrophobic Phospholipid Barrier Is an Early Event in Helicobacter felis-Induced Gastritis in Mice

Abstract

Helicobacter pylori infection has been linked tothe development of gastritis which can then progress toa number of disease entities including peptic ulcerdisease and gastric cancer. Since the pathogenic mechanism by which the bacteria causesgastritis is unresolved, we employed a model system, theH. felis-infected mouse to investigate the temporalrelationship between bacterially-induced alterations in the hydrophobic phospholipid barrier of thestomach and the development of gastritis. In the presentstudy, C57BL/6 mice were inoculated with 10⁹CFU of H. felis and the changes in gastric wet weight, histology, surface hydrophobicity,phospholipid/phosphatidylcholine concentration,phospholipase A₂ activity, and the pH ofcollected gastric juice were measured 0.5-2 monthspostinoculation. In related experiments, we investigated the effects oftreating H. felis infected mice with antibiotic/bismuththerapy on the above gastric properties. It wasdetermined that both gastric surface hydrophobicity and phospholipid composition were significantlyattenuated as early as 2-4 weeks postinfection,preceding signs of mucosal inflammation and glandularatrophy as indicated by increases in gastric wet weight, pH and a disappearance in parietal cells. Theseearly H. felis-induced changes in gastric surfacehydrophobicity and phospholipid concentration werereversed by antibiotic/bismuth therapy. Based on these results we conclude that H. felis infectioninduces an early transformation of the stomach from ahydrophobic to an acid-sensitive hydrophilic state thatmay trigger the subsequent development ofgastritis.