Aims: We have previously shown that H. pylori increases the passage of intact protein across the digestive epithelium, in vitro and in vivo in mice. The aim of this study was to test whether H. pylori can alter gastric permeability to a food-type antigen in humans.
Methods: Antral and corpus gastric biopsies obtained from H. pylori-positive and H. pylori-negative patients suffering from nonulcer dyspepsia with normal esogastroduodenal endoscopy were mounted in adapted Ussing chambers to measure gastric permeability. Electrical resistance (R, an index of epithelial integrity) and fluxes of 14C-mannitol (JMan, a marker of paracellular permeability) and 3H-horseradish peroxidase (HRP, a test protein of antigen transport and processing) under intact (JHRPi) and degraded (JD) form, across the biopsies, were measured.
Results: At the corpus level, biopsies obtained from H. pylori-positive patients, as compared to H. pylori-negative patients, presented significantly higher intact--but not degraded--HRP fluxes (JHRPi = 446 +/- 297 and 219 +/- 265 ng/h cm2, p < 0.05; JD = 4,247 +/- 3,884 and 3,575 +/- 2,594 ng/h x cm2, respectively), and an increase in paracellular permeability (Jman = 0.35 +/- 0.1 vs 0.24 +/- 0.08 micromol/h x cm2, p < 0.02, respectively). At the antrum level, a tendency to increased intact HRP fluxes in H. pylori-positive patients, as compared to H. pylori-negative patients, was observed (JHRPi = 284 +/- 250 vs 207 +/- 203 ng/h x cm2, p < 0.09), without modifications of paracellular permeability.
Conclusions: H. pylori infection increases absorption of an intact food antigen across the corpus gastric mucosa. This phenomenon may contribute to the maintenance of gastric inflammation and could play a role in the development of allergic sensitization to dietary antigens in susceptible individuals.
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