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Porphyromonas gingivalis stimulates IL-18 secretion in human monocytic THP-1 cells

Michael Yee1, Andrew Kim, Tamer Alpagot

  • 1Department of Biomedical Sciences, University of the Pacific, Arthur A. Dugoni School of Dentistry, 2155 Webster Street, San Francisco, CA 94115, USA.

Microbes and Infection
|April 10, 2012
PubMed

Insights

Porphyromonas gingivalis, a key periodontitis pathogen, significantly boosts interleukin-18 (IL-18) secretion in immune cells. This suggests a role for IL-18 in driving chronic gum disease progression.

Area of Science:

  • Oral microbiology
  • Immunology
  • Cytokine research

Background:

  • Porphyromonas gingivalis is a primary etiological agent in chronic periodontitis.
  • Chronic periodontitis is characterized by persistent inflammation and tissue destruction.
  • Interleukin-18 (IL-18) is a pro-inflammatory cytokine involved in immune responses.

Purpose of the Study:

  • To investigate the effect of Porphyromonas gingivalis on interleukin-18 (IL-18) secretion.
  • To determine if live or heat-inactivated P. gingivalis influences IL-18 production in monocytic cells.

Main Methods:

  • Utilized monocytic THP-1 cells (macrophage-like and in suspension).
  • Exposed cells to live and heat-inactivated Porphyromonas gingivalis.
  • Measured interleukin-18 (IL-18) secretion levels using appropriate assays.
  • Assessed the cytotoxic effects of P. gingivalis.

Main Results:

  • Live Porphyromonas gingivalis significantly stimulated IL-18 secretion.
  • Heat-inactivation of P. gingivalis markedly reduced IL-18 stimulation.
  • IL-18 levels after heat-inactivation were comparable to stimulation with P. gingivalis lipopolysaccharide (LPS) alone.
  • Live P. gingivalis exhibited significant cytotoxicity, which was diminished upon heat-inactivation.

Conclusions:

  • Porphyromonas gingivalis actively stimulates the production and release of active IL-18.
  • This P. gingivalis-induced IL-18 release may contribute to the inflammatory processes in periodontitis progression.
  • The findings highlight IL-18 as a potential mediator in P. gingivalis-associated chronic inflammation.

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