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MMP-9/TIMP-1 imbalance induced in human dendritic cells by Porphyromonas gingivalis

Ravi Jotwani1, Sridhar V K Eswaran, Surinder Moonga

  • 1Department of Periodontics and Implantology, Stony Brook University, NY 11794-8703, USA.

FEMS Immunology and Medical Microbiology
|December 25, 2009
PubMed

Insights

Porphyromonas gingivalis components, particularly lipopolysaccharide and fimbriae, strongly induce matrix metalloproteinase-9 (MMP-9) in dendritic cells (DCs). This MMP-9 induction, linked to tissue destruction in periodontitis, is inversely related to IL-10 levels.

Area of Science:

  • Immunology
  • Microbiology
  • Oral Biology

Background:

  • Matrix metalloproteinase-9 (MMP-9) facilitates leukocyte trafficking and tissue remodeling.
  • Unregulated MMP-9 activity, often due to low tissue inhibitor of metalloproteinase-1 (TIMP-1), contributes to tissue destruction.
  • Dendritic cells (DCs) infiltration into oral mucosa increases in chronic periodontitis, associated with pathogens like Porphyromonas gingivalis.

Purpose of the Study:

  • To investigate the role of Porphyromonas gingivalis components in inducing matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in human monocyte-derived dendritic cells (DCs).
  • To compare the effects of P. gingivalis lipopolysaccharide (LPS) and fimbriae with those of Escherichia coli LPS on MMP-9 and interleukin-10 (IL-10) induction.
  • To elucidate the relationship between MMP-9, TIMP-1, and IL-10 induction by P. gingivalis in DCs.

Main Methods:

  • Human monocyte-derived DCs were stimulated with varying doses of P. gingivalis 381 LPS and E. coli 25922 LPS.
  • DCs were also exposed to whole live P. gingivalis 381 strains, including wild-type, major fimbriae mutant (DPG-3), minor fimbriae mutant (MFI), and double mutant (MFB).
  • Levels of MMP-9, TIMP-1, and IL-10 were quantified using multiple measurement techniques.

Main Results:

  • P. gingivalis LPS was a more potent inducer of MMP-9 and a weaker inducer of TIMP-1 compared to E. coli LPS, resulting in a high MMP-9/TIMP-1 ratio.
  • Whole live P. gingivalis strains (wild-type, DPG-3, MFB) potently induced MMP-9, while the MFI mutant showed minimal induction.
  • MMP-9 induction by P. gingivalis components was inversely correlated with IL-10 induction.

Conclusions:

  • P. gingivalis components, including LPS and fimbriae, significantly induce MMP-9 production by DCs.
  • The distinct induction patterns suggest specific roles for LPS and different fimbriae in modulating MMP-9 expression.
  • These findings highlight the potential of P. gingivalis in driving local tissue destruction and leukocyte trafficking via MMP-9 induction in periodontitis.

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