Inhibition of CCL2 by bindarit alleviates diabetes-associated periodontitis by suppressing inflammatory monocyte infiltration and altering macrophage properties
Xu, Hockin H. K.
JournalCellular & Molecular Immunology
PublisherSpringer Science and Business Media LLC
MetadataShow full item record
AbstractDiabetes-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.
SponsorsNational Natural Science Foundation of China
Immunology and Allergy
Identifier to cite or link to this itemhttp://hdl.handle.net/10713/13403
Except where otherwise noted, this item's license is described as https://creativecommons.org/licenses/by/4.0