Attenuation of hydrophobic phospholipid barrier is an early event in Helicobacter felis-induced gastritis in mice

Helicobacter pylori infection has been linked to the development of gastrit is which can then progress to a number of disease entities including peptic ulcer disease and gastric cancer. Since the pathogenic mechanism by which the bacteria causes gastritis is unresolved, we employed a model system, th e H. felis-infected mouse to investigate the temporal relationship between bacterially-induced alterations in the hydrophobic phospholipid barrier of the stomach and the development of gastritis. In the present study, C57BL/6 mice were inoculated with 10(9) CFU of H. felis and the changes in gastric wet weight, histology surface hydrophobicity, phospholipid/phosphatidylcho line concentration, phospholipase A(2) activity, and the pH of collected ga stric juice were measured 0.5-2 months postinoculation. In related experime nts, we investigated the effects of treating H. felis infected mice with an tibiotic/bismuth therapy on the above gastric properties. It was determined that both gastric surface hydrophobicity and phospholipid composition were significantly attenuated as early as 2-4 weeks postinfection, preceding si gns of mucosal inflammation and glandular atrophy as indicated by increases in gastric wet weight, pH and a disappearance in parietal cells. These ear ly H. felis-induced changes in gastric surface hydrophobicity and phospholi pid concentration were reversed by antibiotic/bismuth therapy. Based on the se results we conclude that H. felis infection induces an early transformat ion of the stomach from a hydrophobic to an acid-sensitive hydrophilic stat e that may trigger the subsequent development of gastritis.