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首页> 外文期刊>Infection and immunity >Porphyromonas gingivalis Exacerbates Ligature-Induced, RANKL-Dependent Alveolar Bone Resorption via Differential Regulation of Toll-Like Receptor 2 (TLR2) and TLR4
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Porphyromonas gingivalis Exacerbates Ligature-Induced, RANKL-Dependent Alveolar Bone Resorption via Differential Regulation of Toll-Like Receptor 2 (TLR2) and TLR4

机译：牙龈卟啉单胞菌通过对Toll样受体2（TLR2）和TLR4的差异调节加重了结扎诱导的RANKL依赖性肺泡骨吸收。

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Toll-like receptors (TLRs) play a key role in the innate immune responses to periodontal pathogens in periodontal disease. The present study was performed to determine the roles of TLR2 and TLR4 signaling in alveolar bone resorption, using a Porphyromonas gingivalis-associated ligature-induced periodontitis model in mice. Wild-type (WT), Tlr2?/?, and Tlr4?/? mice (8 to 10 weeks old) in the C57/BL6 background were used. Silk ligatures were applied to the maxillary second molars in the presence or absence of live P. gingivalis infection. Ligatures were removed from the second molars on day 14, and mice were kept for another 2 weeks before sacrifice for final analysis (day 28). On day 14, there were no differences in alveolar bone resorption and gingival RANKL expression between mice treated with ligation plus P. gingivalis infection and mice treated with ligation alone. Gingival interleukin-1β (IL-1β) and tumor necrosis factor alpha (TNF-α) expression was increased, whereas IL-10 expression was decreased in WT and Tlr2?/? mice but not in Tlr4?/? mice. On day 28, WT and Tlr4?/? mice treated with ligation plus P. gingivalis infection showed significantly increased bone loss and gingival RANKL expression compared to those treated with ligation alone, whereas such an increase was diminished in Tlr2?/? mice. Gingival TNF-α upregulation and IL-10 downregulation were observed only in WT and Tlr4?/? mice, not in Tlr2?/? mice. In all mice, bone resorption induced by ligation plus P. gingivalis infection was antagonized by local anti-RANKL antibody administration. This study suggests that P. gingivalis exacerbates ligature-induced, RANKL-dependent periodontal bone resorption via differential regulation of TLR2 and TLR4 signaling.
机译：Toll样受体（TLR）在对牙周病中的牙周病原体的先天免疫应答中起关键作用。进行本研究，以确定牙龈卟啉单胞菌相关结扎诱发的牙周炎模型中TLR2和TLR4信号传导在牙槽骨吸收中的作用。使用野生型（WT），Tlr2 ？/？和Tlr4 ？/？小鼠（8至10周龄）在C57 / BL6背景中。在存在或不存在活牙龈卟啉单胞菌感染的情况下，将丝结扎线施加于上颌第二磨牙。在第14天从第二磨牙中去除结扎，将小鼠再呆2周，然后处死以进行最终分析（第28天）。在第14天，经结扎加牙龈卟啉单胞菌感染治疗的小鼠和仅经结扎处理的小鼠之间的牙槽骨吸收和牙龈RANKL表达没有差异。 WT和Tlr2 ？/？小鼠的牙龈白细胞介素-1β（IL-1β）和肿瘤坏死因子α（TNF-α）表达升高，而IL-10表达降低，而Tlr4 < sup>？/？小鼠。在第28天，与单纯结扎相比，经结扎加牙龈卟啉单胞菌感染治疗的WT和Tlr4 ？/？小鼠显示出骨丢失和牙龈RANKL表达显着增加，而在单独使用结扎法治疗的小鼠中，这种损失有所减少。 Tlr2 ？/？小鼠。仅在WT和Tlr4 ？/？小鼠中观察到牙龈TNF-α上调和IL-10下调，而在Tlr2 ？/？小鼠中未观察到。在所有小鼠中，通过局部抗RANKL抗体施用拮抗由结扎加牙龈假单胞菌感染引起的骨吸收。这项研究表明，牙龈卟啉单胞菌通过对TLR2和TLR4信号的差异调节，加剧了结扎诱导的RANKL依赖性牙周骨吸收。

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