Helicobacter pylori persistently colonize the human stomach and have been linked to
atrophic gastritis and gastric carcinoma. Although it is well known that H. pylori infection can
result in hypochlorhydria, the molecular mechanisms underlying this phenomenon remain
poorly understood. Here we show that VacA permeabilizes the apical membrane of gastric
parietal cells and induces hypochlorhydria. The functional consequences of VacA infection
on parietal cell physiology were studied using freshly isolated rabbit gastric glands and …