Helicobacter pylori Infection and Endothelial Dysfunction

Abstract

Endothelial cells play a critical role in maintaining the integrity of vascular structure and function. Endothelial dysfunction is closely associated with the development and progression of cardiovascular diseases (CVDs) like hypertension (HTN) and atherosclerosis. Gut microorganisms significantly contribute to atherosclerosis and related CVDs. Helicobacter pylori (H. pylori) colonizes in human gastric epithelium in a significant portion of general population in the world. Patients with H. pylori infection have significantly increased risk for CVDs including atherosclerosis, HTN, coronary heart disease, and cerebrovascular disease especially in younger patients (< 65 years old). H. pylori infection significantly impairs vascular endothelial function through multiple mechanisms including increased reactive oxygen species production and oxidative stress, inflammation, decreased nitric oxide formation, modification of the expression of cytokines and microRNAs, abnormalities of lipid and glucose metabolisms, and exosomes-mediated pathways. Endothelial dysfunction associated with H. pylori infection is reversible in both animal model and human subjects. Accumulating data suggests that H. pylori infection is an important risk factor for endothelial dysfunction and CVDs especially in young patients. Screening young male population for H. pylori infection and treating accordingly could be an effective approach for early prevention of CVDs especially premature atherosclerosis associated with H. pylori infection.