Effects of periodontitis induced inflammasome activation on arteriosclerosis and its control

2017 Fiscal Year Final Research Report

• Project/Area Number: 26463145
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Periodontology
• Research Institution: Nihon University
• Principal Investigator: OCHIAI Tomoko (栗田智子) 日本大学, 松戸歯学部, 教授 (20130594)
• Co-Investigator(Renkei-kenkyūsha): OGUCHI Sumito 日本大学, 松戸歯学部, 准教授 (30366611) ; SUZUKI Toshihiko 琉球大学, 医学部, 教授 (10292848)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: 感染 / 歯周病 / 歯周病原細菌 / インフラマソーム / 動脈硬化

Outline of Final Research Achievements

Oral infection of the periodontopathic bacteria P. ginigivalis (P. g.) activate various inflammasomes and induce inflammatory cytokine production, resulting in the production of Th17 cells It was suggested that chronic inflammation may persist due to induction and enhancement of IL-17. Furthermore, it was suggested that gingipain and fimbria, which are the pathogenic factors of P. g., are involved in the activation of these inflammasomes. P. g. or A. a. infection into ApoEshl mice also increased the oxidative denaturation enhancing action of LDL. In vitro experiments, P. g. and P. g. LPS enhanced active oxygen (ROS) production from vascular endothelial cells. Furthermore, it was suggested that P.g. has a common epitope with ox-LDL and may be involved not only in direct oxidation by P.g. but also in inflammation enhancement due to molecular homology.

Free Research Field

医歯薬学