Crosstalk of TLRs in gingival epithelial cells

2015 Fiscal Year Final Research Report

• Project/Area Number: 26893145
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Periodontology
• Research Institution: Osaka University
• Principal Investigator: Mori Kenta 大阪大学, 歯学研究科(研究院), 特任研究員 (40733027)
• Project Period (FY): 2014-08-29 – 2016-03-31
• Keywords: 歯肉上皮細胞 / TLR3 / TLR2

Outline of Final Research Achievements

The necrotic cell supernatant (NCS), functioned as an endogenous danger signal when released from necrotic epithelial cells exposed to repeat freeze thawing, contained RNA and induced the production of inflammatory cytokines including IFN-beta from gingival epithelial cells (epi4) via TLR3. The activation of TLR3 with NCS or Poly(I:C), a strong TLR3 activator, enhanced TLR2 mRNA expression and proteins in epi4. Upregulation of TLR2 in epi4 was induced by TLR3-stimulated IFN-beta by an autocrine/paracrine mechanism. The NCS reduced the expression of epithelial tight junction molecules zona occludens 1 (ZO-1) and occludin and increased the permeability of epithelial tight junctions. These results suggest that endogenous danger signal is involved in the immunopathogenesis of periodontal diseases.

Free Research Field

歯周治療学