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

IF 4.2 2区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Journal of periodontology Pub Date : 2024-08-30 DOI:10.1002/jper.24-0114
Guoqin Cao, Qiuping Xu, Shengyuan Huang, Dong Dai, Jilei Wang, Wei Li, Yue Zhao, Jiang Lin, Xiaozhe Han
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Abstract

BackgroundThe 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.MethodsMacrophages 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.ResultsIn 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, B10 cells inhibit the polarization of CD68+CD86+M1 macrophages and iNOS expression but enhance the polarization of CD68+CD206+M2 macrophages and ARG‐1 expression. Importantly, the depletion of macrophages partially weakened the regulation function of B10 cells in periodontitis.ConclusionsB10 cells promote M2 macrophage polarization, inhibit M1 macrophage polarization in periodontitis, and alleviate periodontitis partially by regulating macrophage polarization.
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B10 细胞调节巨噬细胞极化,缓解牙周炎的炎症和骨质流失
背景巨噬细胞极化为抗炎表型对解决牙周炎症至关重要。有报道称,B10 细胞能在炎症期间调节巨噬细胞的免疫反应,也能在牙周炎中调节炎症。然而,B10细胞在牙周炎中的调节功能是否与巨噬细胞极化有关仍不清楚。本研究旨在探讨B10细胞能否调控牙周炎中巨噬细胞的极化。方法将巨噬细胞与 B10 细胞体外共培养 5 天,共培养后直接或在 Pg-LPS/IFN-γ 或 IL-4/IL-13 刺激下获得巨噬细胞进行分析。采用流式细胞术和/或逆转录聚合酶链反应(RT-PCR)检测巨噬细胞中IL-1β、iNOS、TNF-α、CD206和ARG-1的表达。野生小鼠或巨噬细胞缺失小鼠在结扎后第 5 天转移 B10 细胞。甲苯胺蓝和TRAP染色用于评估牙槽骨吸收和破骨细胞活化。免疫组化用于检测 CD68、IL-1β、TNF-α、iNOS、ARG-1 和 IL-10 的表达。结果在体外,B10 细胞抑制巨噬细胞中 IL-1β、iNOS 和 TNF-α 的表达,同时增加 CD206 和 ARG-1 的表达。在实验性牙周炎中,B10细胞抑制了CD68+CD86+M1巨噬细胞的极化和iNOS的表达,但增强了CD68+CD206+M2巨噬细胞的极化和ARG-1的表达。结论 B10细胞在牙周炎中促进M2巨噬细胞极化,抑制M1巨噬细胞极化,并通过调节巨噬细胞极化部分缓解牙周炎。
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来源期刊
Journal of periodontology
Journal of periodontology 医学-牙科与口腔外科
CiteScore
9.10
自引率
7.00%
发文量
290
审稿时长
3-8 weeks
期刊介绍: The Journal of Periodontology publishes articles relevant to the science and practice of periodontics and related areas.
期刊最新文献
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