Regulation of periodontal disease-related cognitive impairment by controlling microglial phenotype change

2016 Fiscal Year Final Research Report

• Project/Area Number: 26861555
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Functional basic dentistry
• Research Institution: University of Occupational and Environmental Health, Japan (2015-2016); Kyushu University (2014)
• Principal Investigator: Okada Ryo 産業医科大学, 医学部, 講師 (70633105)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: ミクログリア / カテプシンB / 歯周病

Outline of Final Research Achievements

Cathepsin B is a lysosomal cysteine protease, and its expression level is elevated at several immune cell types under inflammatory conditions. To clarify the roles of this enzyme on microglial phenotype change, pro-inflammatory M1 phenotype was induced to microglia, and Cathepsin B mRNA expression level was evaluated. This gene expression level was elevated by stimulation with E.coli LPS, but not changed by stimulation with Interferon-γ. These results indicated that this protease expression is regulated by some particular stimulations.
Next, I examined the possibility that periodontal disease-causing bacterium change mammalian brain cell phenotypes by direct interaction. By brain endothelial cell culture with Porphyromonas gingivalis, various inflammatory cytokines were expressed in this mammalian cell. These results suggested that bacteria sensing brain endothelial cells may induce inflammatory conditions and change some brain cell phenotypes at local area in brain.

Free Research Field

生化学、分子生物学、細胞生物学