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.

中文翻译：

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B10 细胞调节巨噬细胞极化以减轻牙周炎中的炎症和骨质流失


背景巨噬细胞极化为抗炎表型对于解决牙周炎症至关重要。据报道，B10细胞可以调节炎症期间巨噬细胞的免疫反应，也能够调节牙周炎中的炎症。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尚不清楚。本研究旨在探讨B10细胞是否能够调节牙周炎中巨噬细胞极化。方法将巨噬细胞与B10细胞在体外共培养5 d。共培养后，获得巨噬细胞直接用于分析或随后用 Pg-LPS/IFN-γ 或 IL-4/IL-13 刺激。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。 B10 细胞在结扎后第五天转移到野生或巨噬细胞耗竭小鼠中。甲苯胺蓝和TRAP染色用于评估牙槽骨吸收和破骨细胞活化。采用免疫组化法检测CD68、IL-1β、TNF-α、iNOS、ARG-1、IL-10的表达。免疫荧光检测CD68+CD86+M1巨噬细胞和CD68+CD206+M2巨噬细胞的表达。结果体外，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CD206的表达。 ARG-1。在实验性牙周炎中，B10细胞抑制CD68+CD86+M1巨噬细胞的极化和iNOS表达，但增强CD68+CD206+M2巨噬细胞的极化和ARG-1表达。重要的是，巨噬细胞的耗竭部分削弱了B10细胞在牙周炎中的调节功能。结论牙周炎中B10细胞促进M2型巨噬细胞极化，抑制M1型巨噬细胞极化，通过调节巨噬细胞极化部分缓解牙周炎。