Porphyromonas gingivalis accelerates atherosclerosis through oxidation of high-density lipoprotein
10.5051/jpis.2018.48.1.60
- Author:
Hyun Joo KIM
1
;
Gil Sun CHA
;
Hyung Joon KIM
;
Eun Young KWON
;
Ju Youn LEE
;
Jeomil CHOI
;
Ji Young JOO
Author Information
1. Department of Periodontology, Pusan National University School of Dentistry, Yangsan, Korea. joojy@pusan.ac.kr
- Publication Type:Original Article
- Keywords:
Atherosclerosis;
Cardiovascular diseases;
Cholesterol;
Periodontitis;
Porphyromonas gingivalis
- MeSH:
Atherosclerosis;
Cardiovascular Diseases;
Cholesterol;
Foam Cells;
Lipoproteins;
Macrophages;
Monocytes;
Periodontitis;
Porphyromonas gingivalis;
Porphyromonas;
Thiobarbituric Acid Reactive Substances;
Tumor Necrosis Factor-alpha
- From:Journal of Periodontal & Implant Science
2018;48(1):60-68
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: The aim of this study was to evaluate the ability of Porphyromonas gingivalis (P. gingivalis) to induce oxidation of high-density lipoprotein (HDL) and to determine whether the oxidized HDL induced by P. gingivalis exhibited altered antiatherogenic function or became proatherogenic. METHODS: P. gingivalis and THP-1 monocytes were cultured, and the extent of HDL oxidation induced by P. gingivalis was evaluated by a thiobarbituric acid-reactive substances (TBARS) assay. To evaluate the altered antiatherogenic and proatherogenic properties of P. gingivalis-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 P. gingivalis, Oil Red O staining was performed to examine foam cells. RESULTS: P. gingivalis induced HDL oxidation. The HDL treated by P. gingivalis did not reduce lipid oxidation and may have enhanced the formation of MMP-9 and TNF-α. P. gingivalis-treated macrophages exhibited more lipid aggregates than untreated macrophages. CONCLUSIONS: P. gingivalis induced HDL oxidation, impairing the atheroprotective function of HDL and making it proatherogenic by eliciting a proinflammatory response through its interaction with monocytes/macrophages.
