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A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
09:52

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

Published on: August 8, 2014

Porphyromonas gingivalis gingipains trigger a proinflammatory response in human monocyte-derived macrophages through

Daniel Grenier1, Shin-Ichi Tanabe

  • 1Groupe de Recherche en Écologie Buccale, Faculté de Médecine Dentaire, Université Laval, Quebec City, Quebec. daniel.grenier@greb.ulaval.ca

Toxins
|November 10, 2011
PubMed

Insights

Porphyromonas gingivalis gingipains trigger inflammation by activating human macrophages. This suggests gingipains contribute to tissue destruction in chronic periodontitis.

Area of Science:

  • Oral Microbiology
  • Immunology
  • Periodontology

Background:

  • Porphyromonas gingivalis is a key pathogen in chronic periodontitis.
  • Gingipains are major virulence factors produced by P. gingivalis.
  • The role of gingipains in initiating host inflammatory responses remains under investigation.

Purpose of the Study:

  • To investigate the pro-inflammatory capacity of P. gingivalis gingipains.
  • To determine the effect of gingipains on human monocyte-derived macrophages.
  • To elucidate the signaling pathways involved in gingipain-induced macrophage activation.

Main Methods:

  • Human monocyte-derived macrophages were stimulated with purified Arg- and Lys-gingipain preparations.
  • Cytokine secretion (TNF-α, IL-8) was measured.
  • Levels of phosphorylated p38α MAPK were assessed.

Main Results:

  • Both Arg- and Lys-gingipains induced TNF-α and IL-8 secretion.
  • Catalytic activity was not required for gingipain-induced inflammation.
  • Gingipain stimulation increased phosphorylated p38α MAPK, indicating pathway activation.

Conclusions:

  • P. gingivalis Arg- and Lys-gingipains are potent inducers of pro-inflammatory cytokine secretion.
  • Gingipain-mediated inflammation involves the p38α MAPK signaling pathway.
  • These findings highlight gingipains' contribution to periodontitis-associated tissue damage.
Keywords:
P. gingivaliscytokineinflammationmacrophagep38α MAPKproteinase

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