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Organotypic Tissue Model Systems for Investigating Host-Pathogen Interactions In Vitro
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Periodontal Pathogens Promote Foam Cell Formation by Blocking Lipid Efflux.

J H Rho1,2, H J Kim1,2, J Y Joo2,3

  • 1Department of Oral Pathology and BK21 FOUR Project, School of Dentistry, Pusan National University, Yangsan, Republic of Korea.

Journal of Dental Research
|April 26, 2021
PubMed
Summary

Periodontal pathogens promote foam cell formation in atherosclerosis by disrupting lipid homeostasis. This involves increased lipid accumulation, altered cholesterol efflux, and dysregulated calcium (Ca2+) and reactive oxygen species (ROS) signaling.

Keywords:
ATP-binding cassette transporters G1 (ABCG1)Fusobacterium nucleatumPorphyromonas gingivalisfoam cellslipid metabolismmacrophages

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Area of Science:

  • Cardiovascular Research
  • Microbiology
  • Cellular Biology

Background:

  • Foam cells are key components of atherosclerotic plaques.
  • Periodontal pathogens have been detected in plaques, linking periodontitis to cardiovascular disease.
  • The precise role of periodontal pathogens in foam cell formation and associated cellular signaling remains unclear.

Purpose of the Study:

  • To investigate the role of periodontal pathogens in macrophage-to-foam cell transition.
  • To characterize lipid accumulation and identify key molecular players in lipid homeostasis disruption.
  • To explore the involvement of calcium (Ca2+) and reactive oxygen species (ROS) signaling.

Main Methods:

  • Macrophages were infected with periodontal pathogens.
  • Lipid accumulation was assessed using BODIPY 493/503 and Oil Red O staining.
  • Lipid localization, cholesterol ester levels, and signaling molecules (ABCG1, CYP46A1, Ca2+, ROS) were analyzed. Treatments with ROS inhibitors and nifedipine were performed.

Main Results:

  • Periodontal pathogen infection significantly increased neutral lipid and aggregate accumulation in macrophages, localized to the endoplasmic reticulum.
  • Cholesteryl ester levels rose, indicating disrupted lipid homeostasis.
  • Increased Ca2+ signaling and ROS production were observed, alongside altered cholesterol efflux enzymes (ABCG1, CYP46A1). Treatments targeting ROS and Ca2+ signaling reduced lipid droplet accumulation.

Conclusions:

  • Periodontal pathogens drive foam cell formation by inducing lipid homeostasis dysregulation in macrophages.
  • Altered Ca2+ and ROS signaling are critical mediators of this process.
  • Findings highlight a direct link between periodontal infection and the cellular mechanisms underlying atherosclerosis.