Inhibition of CCL2 by bindarit alleviates diabetes-associated periodontitis by suppressing inflammatory monocyte infiltration and altering macrophage properties
Author
Shen, ZongshanKuang, Shuhong
Zhang, Min
Huang, Xin
Chen, Jiayao
Guan, Meiliang
Qin, Wei
Xu, Hockin H. K.
Lin, Zhengmei
Date
2020-07-16Journal
Cellular & Molecular ImmunologyPublisher
Springer Science and Business Media LLCType
Article
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Show full item recordAbstract
Diabetes-associated periodontitis (DP) aggravates diabetic complications and increases mortality from diabetes. DP is caused by diabetes-enhanced host immune-inflammatory responses to bacterial insult. In this study, we found that persistently elevated CCL2 levels in combination with proinflammatory monocyte infiltration of periodontal tissues were closely related to DP. Moreover, inhibition of CCL2 by oral administration of bindarit reduced alveolar bone loss and increased periodontal epithelial thickness by suppressing periodontal inflammation. Furthermore, bindarit suppressed the infiltration of proinflammatory monocytes and altered the inflammatory properties of macrophages in the diabetic periodontium. This finding provides a basis for the development of an effective therapeutic approach for treating DP.Sponsors
National Natural Science Foundation of ChinaKeyword
ImmunologyImmunology and Allergy
Infectious Diseases
bindarit
Diabetes-associated periodontitis
macrophages
proinflammatory monocytes
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http://hdl.handle.net/10713/13403ae974a485f413a2113503eed53cd6c53
10.1038/s41423-020-0500-1
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Except where otherwise noted, this item's license is described as https://creativecommons.org/licenses/by/4.0