Polyamine- and NADPH-dependent generation of ROS during Helicobacter pylori infection: A blessing in disguise

Helicobacter pylori is a Gram-negative bacterium that specifically colonizes the gastric ecological niche. During the infectious process, which results in diseases ranging from chronic gastritis to gastric cancer, the host response is characterized by the activation of the innate immunity of gastric epithelial cells and macrophages. These cells thus produce effector molecules such as reactive oxygen species (ROS) to counteract the infection. The generation of ROS in response to H. pylori involves two canonical pathways: 1) the NADPH-dependent reduction of molecular oxygen to generate O2•−, which can dismute to generate ROS; and 2) the back-conversion of the polyamine spermine into spermidine through the enzyme spermine oxidase, leading to H2O2 production. Although these products have the potential to affect the survival of bacteria, H. pylori has acquired numerous strategies to counteract their deleterious effects. Nonetheless, ROS-mediated oxidative DNA damage and mutations may participate in the adaptation of H. pylori to its ecological niche. Lastly, ROS have been shown to play a major role in the development of the inflammation and carcinogenesis. It is the purpose of this review to summarize the literature about the production of ROS during H. pylori infection and their role in this infectious gastric disease. [Display omitted] •ROS are locally produced in the gastric mucosa during H. pylori infection.•Spermine oxidase and NADPH oxidases are the main sources of ROS in the stomach.•H. pylori has multiple strategies to resist oxidative damage.•ROS-induced mutagenic changes in H. pylori leads to genetic variation and adaptation.•Oxidative stress contributes to H. pylori-induced inflammation and carcinogenesis.