Molecular basis for periodontal medicine based on the interaction between infiltrated inflammatory cells and resident cells.

2016 Fiscal Year Final Research Report

• Project/Area Number: 25293425
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Periodontology
• Research Institution: Kyushu University
• Principal Investigator: NISHIMURA FUSANORI 九州大学, 歯学研究科(研究院), 教授 (80208222)
• Co-Investigator(Kenkyū-buntansha): 浅野 知一郎 広島大学, その他の研究科, 教授 (70242063) ; 山下 明子 九州大学, 大学病院, 助教 (70511319) ; 安孫子 宜光 日本大学, 歯学部, 教授 (70050086) ; 大山 秀樹 兵庫医科大学, 医学部, 准教授 (90280685)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 歯周医学 / 軽微な慢性炎症 / 脂肪細胞－マクロファージ相互作用 / ケモカイン / 脂肪炎症 / 膵島炎症 / 細胞死 / 内毒素

Outline of Final Research Achievements

To understand the molecular basis for the establishment of systemic low-grade inflammation caused by periodontal disease, close interaction between infiltrated macrophages and resident tissue cells was analyzed. Following results were obtained; i) inflammatory adipose tissue expressed chemokine ccl19, and the major source of ccl19 was enlarged adipocyte, 2) mice lacking ccl19 receptor were protected from diet-induced obesity and insulin resistance, 3) these mice were characterized by increased thermogenesis when compared with wild type control mice, 4) when the interaction between infiltrated macrophages and islet resident cells were analyzed, infiltration of endotoxin-activated macrophages up-regulated the expression of apoptosis inducing molecules.

Free Research Field

歯周病学