Infection is thought to be involved in the pathogenesis of
atherosclerosis. Studies have shown the association between helicobacter pylori (H. pylori) and
coronary artery disease. It is interesting to find H. pylori
DNA and
cytotoxin-associated gene A (CagA)
protein in
atherosclerotic plaque. Outer membrane vesicles (OMVs), secreted by H. pylori, exert effects in the distant organ or tissue. However, whether or not OMVs from H. pylori are involved in the pathogenesis of
atherosclerosis remains unknown. Our present study found that treatment with OMVs from CagA-positive H. pylori accelerated
atherosclerosis plaque formation in
ApoE-/- mice. H. pylori-derived OMVs inhibited proliferation and promoted apoptosis of human umbilical vein endothelial cells (HUVECs), which was also reflected in in vivo studies. These effects were normalized to some degree
after treatment with
lipopolysaccharide (LPS)-depleted CagA-positive OMVs or CagA-negative OMVs. Treatment with H. pylori-derived OMVs increased
reactive oxygen species (ROS) levels and enhanced the activation of nuclear factor-κB (NF-κB) in HUVECs, which were reversed to some degree in the presence of a
superoxide dismutase mimetic
TEMPOL and a NF-κB inhibitor
BAY11-7082. Expressions of
interleukin-6 (IL-6) and
tumor necrosis factor alpha (TNF-α), two inflammatory factors, were augmented
after treatment with OMVs from H. pylori. These suggest that H. pylori-derived OMVs accelerate
atherosclerosis plaque formation via endothelium injury. CagA and LPS from H. pylori-OMVs, at least in part, participate in these processes, which may be involved with the activation of ROS/NF-κB signaling pathway. These may provide a novel strategy to reduce the incidence and development of
atherosclerosis.