Helicobacter pylori infection selectively attenuates endothelial function in male mice via exosomes-mediated ROS production.

ABSTRACT:

Background

Substantial sex differences exist in atherosclerosis. Excessive reactive oxygen species (ROS) formation could lead to endothelial dysfunction which is critical to atherosclerosis development and progression. Helicobacter pylori (H. pylori) infection has been shown to attenuate endothelial function via exosomes-mediated ROS formation. We have demonstrated that H. pylori infection selectively increases atherosclerosis risk in males with unknown mechanism(s). The present study was to test the hypothesis that H. pylori infection impaired endothelial function selectively in male mice through exosome-mediated ROS formation.

Methods and results

Age-matched male and female C57BL/6 mice were infected with CagA+ H. pylori to investigate sex differences in H. pylori infectio

SUBMITTER: Zhang L 

PROVIDER: S-EPMC10233065 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature