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Lipoteichoic acid of Enterococcus faecalis inhibitsosteoclastogenesis via transcription factor RBP-J

机译:粪肠球菌的脂磷壁酸抑制通过转录因子RBP-J进行破骨细胞生成

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摘要

Lipoteichoic acid (LTA) of is a potentstimulator of inflammatory responses, but the effects of LTA on osteoclastogenesis remains far from wellunderstood. This study showed that LTAsignificantly inhibited osteoclastogenesis of wild type murine bonemarrow-derived macrophages (BMMs) in the presence of a high dose of RANKL, whilethe inhibition of osteoclastogenesis by LTA wassignificantly removed in BMMs with deficient expression of the transcriptionfactor RBP-J. In addition, a few small osteoclasts were generated in BMMs withonly LTA stimulation, presumably due to theproduction of TNF-α and IL-6. Furthermore, both p38 and ERK1/2 MAPK signalingpathways were activated after 24 h of LTAtreatment, but these signaling pathways were not activated after 6 d oftreatment with RANKL in mature osteoclasts. In conclusion, LTA, which induces inflammatory response, could inhibitRANKL-induced osteoclastogenesis via RBP-J in BMMs.
机译:的脂磷壁酸(LTA)是有效的刺激炎症反应,但LTA对破骨细胞形成的作用仍远未达到了解。这项研究表明LTA显着抑制野生型鼠骨的破骨细胞生成在高剂量的RANKL存在下,骨髓来源的巨噬细胞(BMM),而LTA对破骨细胞的抑制作用为在转录表达不足的BMM中被显着去除RBP-J因子。此外,BMM中还产生了一些小的破骨细胞仅LTA刺激,大概是由于产生TNF-α和IL-6。此外,p38和ERK1 / 2 MAPK信号均LTA 24小时后激活通路治疗,但这些信号通路在6天后未激活RANKL治疗成熟破骨细胞。总之,诱导炎症反应的LTA可以抑制在BMM中,RANKL通过RBP-J诱导破骨细胞生成。

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