Helicobacter pylori causes a lifelong infection and provides a model of bacterial adaptation and persistent colonization. Adenosine is an anti-inflammatory mediator that limits tissue damage during inflammation. We studied the role of adenosine in the T-cell-mediated regulation of gastritis and bacterial persistence.

BACKGROUND & AIMS-Helicobacter pylori-induced gastric epithelial cell (GEC) apoptosis is a complex process that includes activation of the tumor suppressor p53. p53-mediated apoptosis involves p53 activation, bax transcription and cytochrome c release from mitochondria. Apurinic/ apyrimidinic endonuclease-1 (APE-1) regulates transcriptional activity of p53: H. pylori induce APE-1 expression in human GEC. H. pylori infection increases intracellular calcium ion concentration [Ca 2+ ] i of GEC, which iinduces APE-1 acetylation. We investigated the effects of H. pylori infection and APE-1 acetylation on GEC apoptosis.