Porphyromonas gingivalis accelerates atherosclerosis through oxidation of high-density lipoprotein

The aim of this study was to evaluate the ability of ( ) to induce oxidation of high-density lipoprotein (HDL) and to determine whether the oxidized HDL induced by exhibited altered antiatherogenic function or became proatherogenic. and THP-1 monocytes were cultured, and the extent of HDL oxidation induced by was evaluated by a thiobarbituric acid-reactive substances (TBARS) assay. To evaluate the altered antiatherogenic and proatherogenic properties of -treated HDL, lipid oxidation was quantified by the TBARS assay, and tumor necrosis factor alpha (TNF-α) levels and the gelatinolytic activity of matrix metalloproteinase (MMP)-9 were also measured. After incubating macrophages with HDL and , Oil Red O staining was performed to examine foam cells. induced HDL oxidation. The HDL treated by did not reduce lipid oxidation and may have enhanced the formation of MMP-9 and TNF-α. -treated macrophages exhibited more lipid aggregates than untreated macrophages. induced HDL oxidation, impairing the atheroprotective function of HDL and making it proatherogenic by eliciting a proinflammatory response through its interaction with monocytes/macrophages.