Switched memory B cells promote alveolar bone damage during periodontitis: An adoptive transfer experiment
Switched memory B cells promote alveolar bone damage during periodontitis: An adoptive transfer experiment
复制标题
转换记忆 B 细胞在牙周炎期间促进牙槽骨损伤：过继转移实验。
DOI：
10.1016/j.intimp.2018.07.003
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发表时间：
2018-09-01
影响因子：
5.6
通讯作者：
Lin, Xiaoping
中科院分区：
文献类型：
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作者：
Han, Yakun;Jin, Ying;Lin, Xiaoping
牙周炎是一种细菌引起的疾病，通常会导致牙槽骨损伤。我们试图确定开关记忆B细胞在牙周炎牙槽骨破坏中的作用和机制。分选并培养致敏的B细胞，检测其核因子-κ B配体受体激活因子（RANKL）、白细胞介素-6（IL-6）、白细胞介素-12（IL-12）的表达。使用这些细胞，我们准备了过继转移模型，我们诱导牙周炎。我们发现，转换记忆B细胞产生更多的RANKL的蛋白质和mRNA水平比其他亚群。转换记忆B细胞表达IL-6和IL-12 mRNA，但各自的蛋白水平差异不显著。此外，我们发现，转换记忆B细胞转移导致牙槽骨丢失和牙周破骨细胞生成增加。此外，转换记忆B细胞转移增加了Th 1和Th 17细胞的比例以及牙龈和颈部淋巴结（CLN）中RANKL、骨保护素（OPG）、肿瘤坏死因子-α（TNF-α）、干扰素-γ（IFN-γ）、IL-1 β、IL-6、IL-17 A的表达。本研究的结果表明，转换记忆B细胞通过增强细胞因子表达和增加Th 1和Th 17细胞增殖来调节牙槽骨稳态。
Periodontitis is a bacteria-induced disease that often leads to alveolar bone damage. We sought to determine the role and mechanism of switched memory B cells in alveolar bone destruction during periodontitis. Sensitized B cells were sorted and cultured, then their expression of receptor activator for nuclear factor-kappa B ligand (RANKL), interleukin-6 (IL-6), and interleukin-12 (IL-12) was detected. Using these cells, we prepared adoptive transfer models in which we induced periodontitis. We found that switched memory B cells produced more RANKL in terms of both protein and mRNA levels than other subpopulations. Switched memory B cells expressed more IL-6 and IL-12 mRNA than other subpopulations, but differences in respective protein levels were not significant. Moreover, we found that switched memory B cell transfer resulted in increased alveolar bone loss and periodontal osteoclastogenesis. Moreover, switched memory B cell transfer increased the proportion of Th1 and Th17 cells as well as the expression of RANKL, osteoprotegerin (OPG), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), IL-1 beta, IL-6, IL-17A in gingiva, and cervical lymph nodes (CLNs). The outcomes of the present study indicate that switched memory B cells regulate alveolar bone homeostasis via enhancing cytokine expression and increasing proliferation of Th1 and Th17 cells.