Elucidation for the mechanisms of the periodontitis-induced pathogenesis of chronic obstructive pulmonary disease

2020 Fiscal Year Final Research Report

• Project/Area Number: 18K09783
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 57060:Surgical dentistry-related
• Research Institution: Tohoku University
• Principal Investigator: MIZUTA KENTARO 東北大学, 歯学研究科, 教授 (40455796)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Keywords: 慢性閉塞性肺疾患 / 短鎖脂肪酸受容体 / 気管平滑筋

Outline of Final Research Achievements

Emerging evidence suggests that oral microbiota-derived short-chain fatty acids (SFCAs) are important modulators of pathogenesis of chronic obstructive pulmonary disease (COPD). However, it was unclear how periodontitis induces COPD. Therefore, we examined whether SCFAs modulates human airway smooth muscle tone through short chain fatty acid receptor FFAR3, and its intracellular mechanisms. Activation of FFAR3 in human airway smooth muscle with SCFAs potentiated acetylcholine-induced human airway smooth muscle contraction through the reduction of cAMP production and the increase in intracellular calcium.

Free Research Field

歯科麻酔学

Academic Significance and Societal Importance of the Research Achievements

近年、歯周病が全身疾患の増悪に寄与するとのデータが集積しつつ有り注目を集めている。歯周病は慢性閉塞性肺疾患（COPD）の発症・増悪因子としても注目されており、両者の相関性を示唆する疫学的知見が集積しつつあるものの、その病態生理機構は不明であった。本研究は、歯周病原細菌から産生される短鎖脂肪酸が、気管平滑筋上に発現する短鎖脂肪酸受容体FFAR3を介して気管収縮作用をもたらしCOPD症状の増悪に寄与することを明らかにしたものである。