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2022 Fiscal Year Final Research Report

Elucidation of the Mechanism of Diabetic Nephropathy Development Involving Periodontal Bacteria

Research Project

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Project/Area Number 20K09909
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 57020:Oral pathobiological science-related
Research InstitutionKagoshima University

Principal Investigator

Ohnishi Tomokazu  鹿児島大学, 医歯学域歯学系, 准教授 (30244247)

Project Period (FY) 2020-04-01 – 2023-03-31
Keywords歯周炎 / IgA腎症 / 腎糸球体 / IgA / Treponema / メサンギウム細胞
Outline of Final Research Achievements

We established an experimental mouse model of periodontitis induced by Treponema infection to investigate the synergistic effect of periodontal bacterial infection and type 2 diabetes in IgA nephropathy. Wild-type mice were fed a high-fat diet for 4 months and then administered Treponema. As a result, we observed an increase in urinary albumin, IgG, and IgA levels, expansion of the mesangial area, and IgA deposition. To investigate the signaling molecule Tpl2 as a mediator of periodontal bacterial stimulation, we performed the same treatment on Tpl2 knockout mice and found no increase in urinary IgG or IgA levels, and no expansion of the mesangial area or IgA deposition. These findings suggest that Tpl2 plays an important role in the development of IgA nephropathy in the context of the synergistic effect of periodontal bacterial infection and type 2 diabetes.

Free Research Field

口腔生化学

Academic Significance and Societal Importance of the Research Achievements

IgA腎症の治療方法として扁桃摘出が確立されており、その摘出された扁桃の臨床研究から、Treponemaの扁桃への感染が予後に関わる因子として報告されている。また、糖尿病性腎症と言われている腎疾患の多くはIgA腎症に関わりが深いことが知られている。しかし、糖尿病モデルマウスから派生したIgA腎症モデルは報告がない。そこで、本研究では二型糖尿病発症マウスにTreponema を投与し、実験的歯周炎を誘導することでIgA腎症を発症するマウスモデルを確率的に作製した。さらに、このモデルを用いどのような遺伝子欠損がgA腎症発症に関わるかを示した。

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Published: 2024-01-30  

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