Shuto T, Jimi E, Kukita T, Hirata M, Koga T
Department of Biochemistry, Faculty of Dentistry, Kyushu University, Fukuoka, Japan.
Endocrinology. 1994 Feb;134(2):831-7. doi: 10.1210/endo.134.2.8299579.
Lipopolysaccharide (LPS) is a potent bone resorbing factor. We investigated the effect of LPS on osteoclast formation in three types of cultures. LPS inhibited osteoclast formation induced by 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], in a dose-dependent manner, in cultures of whole bone marrow cells without dexamethasone. LPS increased the amount of granulocyte-macrophage colony stimulating factor (GM-CSF) in the culture supernatant, and anti-GM-CSF antiserum almost abolished the inhibition of osteoclast formation by LPS, thereby indicating that GM-CSF generated by treatment with LPS may be responsible for the inhibition of osteoclast formation. In cultures with dexamethasone, the amount of GM-CSF was decreased to one-third of that with 1,25(OH)2D3 alone and was not changed by treatment with LPS. In this culture system, LPS enhanced osteoclast formation. In the coculture system of nonadherent bone marrow cells and a stromal cell line in the presence of 1,25(OH)2D3 and dexamethasone, where no detectable GM-CSF was present in the supernatant, LPS markedly enhanced osteoclast formation, whereas exogenously added GM-CSF (100 pg/ml) almost completely inhibited osteoclast formation. LPS stimulated pit formation on dentin slices by the osteoclast-like cells formed by in vitro culture system.
脂多糖（LPS）是一种强效的骨吸收因子。我们在三种培养体系中研究了LPS对破骨细胞形成的影响。在不含地塞米松的全骨髓细胞培养中，LPS以剂量依赖的方式抑制1,25-二羟基维生素D3[1,25(OH)2D3]诱导的破骨细胞形成。LPS增加了培养上清液中粒细胞-巨噬细胞集落刺激因子（GM-CSF）的量，抗GM-CSF抗血清几乎消除了LPS对破骨细胞形成的抑制作用，从而表明LPS处理产生的GM-CSF可能是破骨细胞形成受抑制的原因。在地塞米松存在的培养体系中，GM-CSF的量降至仅用1,25(OH)2D3时的三分之一，且LPS处理未使其改变。在该培养体系中，LPS增强了破骨细胞的形成。在1,25(OH)2D3和地塞米松存在下，非贴壁骨髓细胞与基质细胞系的共培养体系中，上清液中未检测到GM-CSF，LPS显著增强破骨细胞形成，而外源性添加GM-CSF（100 pg/ml）几乎完全抑制破骨细胞形成。LPS刺激体外培养体系形成的破骨细胞样细胞在牙本质切片上形成陷窝。
