1 Department of Stomatology, The Affiliated Hospital of Qingdao University, School of Stomatology of Qingdao University, Qingdao, China.
2 Endodontology, Faculty of Dentistry, The University of Hong Kong, Hong Kong SAR, China.
Innate Immun. 2019 Jan;25(1):13-21. doi: 10.1177/1753425918812646. Epub 2018 Nov 21.
Lipoteichoic acid (LTA) of Enterococcus faecalis is a potent stimulator of inflammatory responses, but the effects of E. faecalis LTA on osteoclastogenesis remains far from well understood. This study showed that E. faecalis LTA significantly inhibited osteoclastogenesis of wild type murine bone marrow-derived macrophages (BMMs) in the presence of a high dose of RANKL, while the inhibition of osteoclastogenesis by E. faecalis LTA was significantly removed in BMMs with deficient expression of the transcription factor RBP-J. In addition, a few small osteoclasts were generated in BMMs with only E. faecalis LTA stimulation, presumably due to the production of TNF-α and IL-6. Furthermore, both p38 and ERK1/2 MAPK signaling pathways were activated after 24 h of E. faecalis LTA treatment, but these signaling pathways were not activated after 6 d of treatment with RANKL in mature osteoclasts. In conclusion, E. faecalis LTA, which induces inflammatory response, could inhibit RANKL-induced osteoclastogenesis via RBP-J in BMMs.
肠球菌脂磷壁酸（LTA）是一种强烈的炎症反应刺激物，但肠球菌 LTA 对破骨细胞生成的影响还远未被充分理解。本研究表明，在高浓度 RANKL 存在的情况下，肠球菌 LTA 可显著抑制野生型鼠骨髓来源巨噬细胞（BMM）的破骨细胞生成，而在转录因子 RBP-J 表达缺陷的 BMM 中，肠球菌 LTA 对破骨细胞生成的抑制作用则明显消除。此外，在仅用肠球菌 LTA 刺激的 BMM 中也会产生少量小的破骨细胞，这可能是由于 TNF-α 和 IL-6 的产生。此外，在肠球菌 LTA 处理 24 小时后，p38 和 ERK1/2 MAPK 信号通路被激活，但在成熟破骨细胞中用 RANKL 处理 6 天后，这些信号通路并未被激活。总之，肠球菌 LTA 可诱导炎症反应，通过 BMM 中的 RBP-J 抑制 RANKL 诱导的破骨细胞生成。
