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Isolation, Processing and Analysis of Murine Gingival Cells
09:47

Isolation, Processing and Analysis of Murine Gingival Cells

Published on: July 2, 2013

Signaling pathways in osteoblast proinflammatory responses to infection by Porphyromonas gingivalis

T Ohno1, N Okahashi, I Morisaki

  • 1Department of Oral Frontier Biology, Osaka University Graduate School of Dentistry, Suita-Osaka, Japan.

Oral Microbiology and Immunology
|February 19, 2008
PubMed
Abstract

Insights

Porphyromonas gingivalis infection triggers inflammatory responses in stromal and osteoblast cells. These responses are largely dependent on nuclear factor-kappaB (NF-kappaB) but not always on the MyD88 pathway, with some linked to protease-activated receptors.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Periodontal pathogen Porphyromonas gingivalis induces proinflammatory gene expression in mouse stromal cells.
  • Investigated signaling pathways mediating these inflammatory responses.

Purpose of the Study:

  • Elucidate signaling pathways involved in P. gingivalis-induced inflammation in stromal and osteoblast cells.
  • Determine the role of NF-kappaB, MyD88, and protease-activated receptors in these responses.

Main Methods:

  • Infection of ST2 cells and osteoblasts with P. gingivalis and its mutant.
  • Quantification of chemokine and MMP9 expression via real-time PCR.
  • Analysis of protein kinase phosphorylation, IkappaB-alpha degradation, and transcription factor activation using Western blotting and luciferase assays.
  • Assessment of inhibitor effects on signaling pathways.

Main Results:

  • P. gingivalis infection upregulated CCL5, CXCL10, and MMP9 in ST2 cells and osteoblasts.
  • Activation of nuclear factor-kappaB (NF-kappaB) and activator protein-1 transcription factors was observed.
  • NF-kappaB inhibition suppressed CCL5 and MMP9 but not CXCL10 expression.
  • CCL5 expression was induced in MyD88-deficient osteoblasts, and CXCL10 induction was linked to protease-activated receptors.

Conclusions:

  • Proinflammatory responses in P. gingivalis-infected cells are predominantly NF-kappaB-dependent.
  • These responses are not solely reliant on the Toll-like receptor/MyD88 pathway.
  • Protease-activated receptor activation contributes to certain inflammatory pathways, indicating P. gingivalis may bypass typical pathogen recognition molecules.

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