Islam Shamima, Hassan Ferdaus, Tumurkhuu Gantsetseg, Dagvadorj Jargalsaikhan, Koide Naoki, Naiki Yoshikazu, Mori Isamu, Yoshida Tomoaki, Yokochi Takashi
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan.
Biochem Biophys Res Commun. 2007 Aug 24;360(2):346-51. doi: 10.1016/j.bbrc.2007.06.023. Epub 2007 Jun 12.
Lipopolysaccharide (LPS) is a potent bone resorbing factor. The effect of LPS on osteoclast formation was examined by using murine RAW 264.7 macrophage cells. LPS-induced the formation of multinucleated giant cells (MGC) in RAW 264.7 cells 3 days after the exposure. MGCs were positive for tartrate-resistant acid phosphatase (TRAP) activity. Further, MGC formed resorption pits on calcium-phosphate thin film that is a substrate for osteoclasts. Therefore, LPS was suggested to induce osteoclast formation in RAW 264.7 cells. LPS-induced osteoclast formation was abolished by anti-tumor necrosis factor (TNF)-alpha antibody, but not antibodies to macrophage-colony stimulating factor (M-CSF) and receptor activator of nuclear factor (NF)-kappaB ligand (RANKL). TNF-alpha might play a critical role in LPS-induced osteoclast formation in RAW 264.7 cells. Inhibitors of NF-kappaB and stress activated protein kinase (SAPK/JNK) prevented the LPS-induced osteoclast formation. The detailed mechanism of LPS-induced osteoclast formation is discussed.
脂多糖（LPS）是一种强效的骨吸收因子。利用小鼠RAW 264.7巨噬细胞研究了LPS对破骨细胞形成的影响。暴露3天后，LPS诱导RAW 264.7细胞中多核巨细胞（MGC）的形成。MGC对耐酒石酸酸性磷酸酶（TRAP）活性呈阳性。此外，MGC在作为破骨细胞底物的磷酸钙薄膜上形成吸收陷窝。因此，提示LPS可诱导RAW 264.7细胞中的破骨细胞形成。抗肿瘤坏死因子（TNF）-α抗体可消除LPS诱导的破骨细胞形成，但抗巨噬细胞集落刺激因子（M-CSF）和核因子（NF）-κB受体激活剂配体（RANKL）的抗体则不能。TNF-α可能在LPS诱导RAW 264.7细胞破骨细胞形成中起关键作用。NF-κB和应激激活蛋白激酶（SAPK/JNK）抑制剂可阻止LPS诱导的破骨细胞形成。本文讨论了LPS诱导破骨细胞形成的详细机制。
