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Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells
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[Porphyromonas gingivalis infection enhanced the adhesion of monocytes to endothelial]

Caixia Zhang1, Jie Song1, Jingjing Li1

  • 1Department of Cell Biology and Genetics, Medical School of Nanjing University, Jiangsu Key Laboratory of Molecular Medicine, Nanjing 210093, China.

Zhonghua Kou Qiang Yi Xue Za Zhi = Zhonghua Kouqiang Yixue Zazhi = Chinese Journal of Stomatology
|May 14, 2014
PubMed
Abstract

Insights

Porphyromonas gingivalis (Pg) infection significantly increases monocyte adhesion to endothelial cells. This Pg-induced inflammation suggests a role in atherosclerosis development.

Area of Science:

  • Oral Microbiology
  • Immunology
  • Cardiovascular Research

Background:

  • Porphyromonas gingivalis (Pg) is implicated in periodontal disease.
  • Monocyte adhesion to endothelial cells is a key event in early atherosclerosis.

Purpose of the Study:

  • To investigate if Porphyromonas gingivalis (Pg) infection enhances monocyte (THP-1) adhesion to human umbilical vein endothelial cells (HUVEC).

Main Methods:

  • THP-1 cells were infected with Pg at a multiplicity of infection of 1:100 for 8 and 24 hours.
  • Co-culture assays were performed to measure THP-1 adhesion to HUVEC.
  • Enzyme-linked immunosorbent assay (ELISA) quantified ICAM-1, MCP-1, and IL-8 expression.

Main Results:

  • Pg infection significantly enhanced THP-1 adhesion to HUVEC by 13.8%-35.2% (P = 0.006) after 24 hours.
  • Intercellular adhesion molecule-1 (ICAM-1) expression on HUVEC increased significantly (P = 0.005).
  • Monocyte chemotactic protein 1 (MCP-1) and interleukin 8 (IL-8) levels were elevated post-Pg infection (P = 0.012 and P = 0.002, respectively).

Conclusions:

  • Pg infection promotes monocyte adhesion to endothelial cells.
  • Pg infection stimulates inflammatory responses, indicated by increased cytokine and adhesion molecule expression.
  • Pg infection may be a risk factor contributing to atherosclerosis development.

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