细菌脂多糖促进RANKL预处理的破骨前体细胞转向成熟分化的调节作用  

Stimulation of osteoclast differentiation by lipopolysaccharide

作　　者：赵为公[1] 王莹[1] 邱希江[1] 白斌[1] 邱裕生[1] 

机构地区：[1]西安交通大学医学院第一附属医院骨科,陕西西安710061

出　　处：《西安交通大学学报（医学版）》2013年第1期42-45,共4页Journal of Xi’an Jiaotong University（Medical Sciences）

摘　　要：目的研究细菌脂多糖(LPS)直接促进破骨细胞分化的调节作用。方法建立RANKL和M-CSF诱导骨髓单核细胞分化为成熟破骨细胞的体外培养方法;采用抗酒石酸酸性磷酸酶染色(TRAP)观察LPS对RANKL预处理的破骨细胞前体分化调节作用;RT-PCR检测LPS对RANKL预处理的破骨细胞前体表达TNF-α、IL-1β。结果 LPS通过刺激破骨前体细胞表达和分泌TNF-α、IL-1β促进破骨细胞向成熟分化,并且不依赖于RANKL-RANK途径。结论 LPS促进RANKL预处理的破骨细胞前体向成熟分化的途径可能是通过增加其自分泌TNF-α和IL-1β完成的。Objective To study the stimulation of osteoclast differentiation by lipopolysaccharide （LPS）. Methods Osteoclasts were prepared in the presence of receptor activator of nuclear factor-κB ligand （RANKL） and macrophage colony-stimulating factor （M-CSF） from bone marrow mononuclear cells; tartrate-resistant acid phosphatase （TRAP） staining was used to observe osteoclastogenic activity induced by lipopolysaccharide （LPS）; RT-PCR was applied to detecte tumor necrosis factor-α （TNF-α） and interleukin 1β （IL-1β） expressions in RANKL- pretreated precursor osteoclasts. Results LPS could induce osteoclast differentiation in RANKL-pretreated precursor osteoclasts and was independent of RANKL-RANK pathway. LPS induced the expression of TNF-a and IL-1β in osteoclast precursors no matter whether they were pretreated with RANKL or not, and these cytokines mediated LPS effect in an autocrine mechanism. Conclusion LPS stimulates osteoclastogenesis in RANKL-pretreated cells by increasing the secretion of TNF-α and IL-1β.

关 键 词：破骨细胞 肿瘤坏死因子-α 脂多糖 核因子-ΚB受体活化因子配体 白细胞介素-1Β 

分 类 号：R392.12[医药卫生—免疫学]