Journal of Periodontal and Implant Science

Korean Academy of Periodontology (대한치주과학회)
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Porphyromonas gingivalis accelerates atherosclerosis through oxidation of high-density lipoprotein

  • Kim, Hyun-Joo (Department of Periodontology, Pusan National University School of Dentistry) ;
  • Cha, Gil Sun (Department of Periodontology, Pusan National University School of Dentistry) ;
  • Kim, Hyung-Joon (Department of Oral Physiology, Institute of Translational Dental Sciences, Pusan National University School of Dentistry) ;
  • Kwon, Eun-Young (Dental Clinic Center, Pusan National University Hospital) ;
  • Lee, Ju-Youn (Department of Periodontology, Pusan National University School of Dentistry) ;
  • Choi, Jeomil (Department of Periodontology, Pusan National University School of Dentistry) ;
  • Joo, Ji-Young (Department of Periodontology, Pusan National University School of Dentistry)
  • Received : 2018.01.26
  • Accepted : 2018.02.21
  • Published : 2018.02.28
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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. gingivalistreated HDL, lipid oxidation was quantified by the TBARS assay, and tumor necrosis factor alpha (TNF-${\alpha}$) 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-${\alpha}$. P. gingivalistreated 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.

Keywords

References

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