[Hyperlipidemia inhibited inflammatory response to Porphyromonas gingivalis in apolipoprotein E knockout mice]

Shanghai Kou Qiang Yi Xue. 2014 Aug;23(4):409-12.
[Article in Chinese]

Abstract

Purpose: To investigate the effect and mechanism of hyperlipidemia on inflammatory response to Porphyromonas gingivalis(P. gingivalis) in apolipoprotein E knock out(ApoE-/-) mice.

Methods: Long term hyperlipidemia model was established in ApoE-/- mice, and viable P. gingivalis were injected into peritoneal cavity to make peritonitis model. Bacteria clearance capability was detected by serial dilution, production of pro-inflammatory cytokine interleukin-6 (IL-6) and monocyte chemotactic protein-1 (MCP-1) in serum was measured by ELISA, and IL-6 as well as MCP-1 transcription in peritoneal cells was determined by real time PCR. The data was analyzed with SPSS13.0 software package.

Results: Hyperlipidemia disrupted P. gingivalis clearance capability in ApoE-/- mice, accompanied by inhibited IL-6 and MCP-1 transcription in peritoneal cells and decreased IL-6 and MCP-1 release into blood.

Conclusions: Hyperlipidemia disrupts inflammatory response to P. gingivalis, leading to decreased bacteria clearance, which may affect periodontitis progression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apolipoproteins
  • Cells, Cultured*
  • Chemokine CCL2
  • Hyperlipidemias
  • Mice
  • Mice, Knockout
  • Periodontitis
  • Porphyromonas gingivalis*

Substances

  • Apolipoproteins
  • Chemokine CCL2