No evidence of a role for mitochondrial complex I in Helicobacter pylori pathogenesis

Background Complex I is the first enzyme complex in the mitochondrial respiratory chain, responsible for generating a large fraction of energy during oxidative phosphorylation. Recently, it has been identified that complex I deficiency can result in increased inflammation due to the generation of reactive oxygen species by innate immune cells. As a reduction in complex I activity has been demonstrated in human stomachs with atrophic gastritis, we investigated whether complex I deficiency could influence Helicobacter pylori pathogenesis. Materials and Methods Ndufs6 gt / gt mice have a partial complex I deficiency. Complex I activity was quantified in the stomachs and immune cells of Ndufs6 gt / gt mice by spectrophotometric assays. Ndufs6 gt / gt mice were infected with H. pylori and bacterial colonization assessed by colony‐forming assay, gastritis assessed histologically, and H. pylori ‐ specific humoral response quantified by ELISA . Results The immune cells and stomachs of Ndufs6 gt / gt mice were found to have significantly decreased complex I activity, validating the model for assessing the effects of complex I deficiency in H. pylori infection. However, there was no observable effect of complex I deficiency on either H. pylori colonization, the resulting gastritis, or the humoral response. Conclusions Although complex I activity is described to suppress innate immune responses and is decreased during atrophic gastritis in humans, our data suggest it does not affect H. pylori pathogenesis.