B10 cells regulate macrophage polarization to alleviate inflammation and bone loss in periodontitis

作者：Guoqin Cao, Qiuping Xu, Shengyuan Huang, Dong Qin Dai, Jilei Wang, Wei Li, Yue Zhao, Jiang Lin, Xiaozhe Han · 发表于：Journal of Periodontology · 年份：2024 · DOI：10.1002/jper.24-0114 · 被引用次数：15 · 研究领域：Oral microbiology and periodontitis research、Immune cells in cancer、Bone and Dental Protein Studies

Abstract Background The polarization of macrophages into an anti‐inflammatory phenotype is crucial for resolving periodontal inflammation. It has been reported that B10 cells can regulate the immune response of macrophages during inflammation and are also able to regulate inflammation in periodontitis. However, whether B10 cells’ regulation function in periodontitis is related to macrophage polarization remains unclear. This study aims to investigate whether B10 cells can regulate macrophage polarization in periodontitis. Methods Macrophages were cocultured with B10 cells in vitro for 5 days. After coculture, macrophages were obtained for analysis directly or followed by stimulation with Pg‐LPS/IFN‐γ or IL‐4/IL‐13. Flow cytometry and/or reverse transcriptase‐polymerase chain reaction (RT‐PCR) were employed to detect the expression of IL‐1β, iNOS, TNF‐α, CD206, and ARG‐1 in macrophages. B10 cells were transferred on the 5th day after ligation in wild or macrophage‐depletion mice. Toluidine blue and TRAP staining were used to evaluate alveolar bone resorption and osteoclast activation. Immunohistochemistry was employed to detect the expression of CD68, IL‐1β, TNF‐α, iNOS, ARG‐1, and IL‐10. Immunofluorescence was used to detect the expression of CD68 + CD86 + M1 macrophages and CD68 + CD206 + M2 macrophages. Results In vitro, B10 cells inhibit the expression of IL‐1β, iNOS, and TNF‐α in macrophages while increasing the expression of CD206 and ARG‐1. In experimental periodontitis...