Wang Yuan, Liu Xin, Dou Ce, Cao Zhen, Liu Chuan, Dong Shiwu, Fei Jun
Center of Trauma of Daping Hospital, Third Military Medical University, Chongqing, China.
Department of Biomedical Materials Science, School of Biomedical Engineering, Third Military Medical University, Chongqing, China.
J Cell Physiol. 2017 Sep;232(9):2396-2406. doi: 10.1002/jcp.25774. Epub 2017 Mar 31.
Bone infection is a common and serious complication in the orthopedics field, which often leads to excessive bone destruction and non-union. Osteoclast is the only type of cells which have the function of bone resorption. Its over activation is closely related to excessive bone loss. Staphylococcus aureus (S. aureus) is a major pathogen causing bone infection, which can produce a large number of strong pathogenic substances staphylococcal protein A (SPA). However, few studies were reported about the effects of SPA on osteoclastogenesis. In our study, we observed that S. aureus activated osteoclasts and promoted bone loss in bone infection specimens. Then, we investigated the effects of SPA on RANKL-induced osteoclastogenesis in vitro, the results revealed that SPA promoted osteoclastic differentiation and fusion, and enhanced osteoclastic bone resorption. In addition, we also showed that SPA upregulated the expression of NFATc1 and c-FOS through the activation of MAPK signaling to promote osteoclastogenesis. Our findings might help us better understand the pathogenic role of S. aureus in bone infection and develop new therapeutic strategies for infectious bone diseases.
骨感染是骨科领域常见且严重的并发症，常导致过度的骨质破坏和骨不连。破骨细胞是唯一具有骨吸收功能的细胞类型。其过度活化与骨质过度流失密切相关。金黄色葡萄球菌是引起骨感染的主要病原菌，可产生大量强致病性物质葡萄球菌蛋白A（SPA）。然而，关于SPA对破骨细胞生成的影响，报道较少。在我们的研究中，我们观察到金黄色葡萄球菌在骨感染标本中激活破骨细胞并促进骨质流失。然后，我们研究了SPA对体外RANKL诱导的破骨细胞生成的影响，结果显示SPA促进破骨细胞分化和融合，并增强破骨细胞的骨吸收。此外，我们还表明SPA通过激活MAPK信号上调NFATc1和c-FOS的表达以促进破骨细胞生成。我们的研究结果可能有助于我们更好地理解金黄色葡萄球菌在骨感染中的致病作用，并为感染性骨病开发新的治疗策略。
