2017 Fiscal Year Final Research Report
The effect of calprotectin on mechanism of progression of diabetes-associated periodontitis
| Project/Area Number |
15K20621
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Periodontology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | カルプロテクチン / 糖尿病関連歯周炎 / TLR4 / IL-6 / THP-1 / sIL-6R |
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| Outline of Final Research Achievements |
Diabetic patients are susceptible to severe periodontitis, but the precise mechanism is not well understood. Purpose of this study was to investigate the biological pathogenesis of severe periodontitis in diabetic patients focusing on calprotectin (CPT) effects in human gingival fibroblasts (HGFs) and macrophages crosstalk.The results were as follows:1. CPT increased significantly IL-6 production via TLR4-NF-κB pathway in HGFs.2. High glucose increased significantly sIL-6R production via Tace activation in THP-1 macrophages.
These results support that diabetic conditions such as HG may induce sIL-6R production from macrophages and may exacerbate the periodontitis synergistically via CPT-induced IL-6 production in HGFs. CPT or HG-induced IL-6 cascades surrounding HGFs may lead in periodontitis progression through the crosstalk of fibroblasts-macrophages. This pathway could be an attractive target to clarify the pathogenesis of severe periodontitis in diabetic patients.
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| Free Research Field |
歯周病学
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