PMC

H. pylori-infected macrophages produces H₂O₂ from L-arginine. H. pylori induces SLC7A2 expression allowing the uptake of L-arginine in macrophages. The induction of ARG2, ODC, which requires a MYC-dependent pathway, and SMOX leads to the release of H₂O₂.

Biochemical pathways used by H. pylori to counteract ROS. The enzyme KatA is transported to the periplasm by the action of KapA and the Tat system. O₂^•− is converted into H₂O by SodB and KatA. Hydroperoxides, peroxynitrites, and H₂O₂ are reduced by the Prx/TrxA system. NapA protects H. pylori from DNA oxidation by an unknown mechanism. NpH and MutS are involved in oxidative DNA repair.

Regulation of NOX by H. pylori. NOX1 is induced in gastric epithelial cells through a PI3K/RAC1 signaling pathway; in these cells, the production of O₂^•− stimulate the expression of APEX that blocks RAC1. In myeloid cells, the expression of NOX2 requires a NapA/PI3K signals. DUOX2 has been shown to be induced in the gastric tissue of infected animals, but the subcellular localization of this enzyme remains unknown. PHD, peroxidase homology domain.