Surface-associated protein from Staphylococcus aureus stimulates osteoclastogenesis: possible role in S. aureus-induced bone pathology.

S Meghji, S J Crean, P A Hill, M Sheikh, S P Nair, K Heron, B Henderson, E B Mawer, M Harris
{"title":"Surface-associated protein from Staphylococcus aureus stimulates osteoclastogenesis: possible role in S. aureus-induced bone pathology.","authors":"S Meghji,&nbsp;S J Crean,&nbsp;P A Hill,&nbsp;M Sheikh,&nbsp;S P Nair,&nbsp;K Heron,&nbsp;B Henderson,&nbsp;E B Mawer,&nbsp;M Harris","doi":"10.1093/rheumatology/37.10.1095","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Staphylococcus aureus is the cause of bone destruction in osteomyelitis, bacterial arthritis and orthopaedic implant failure. We have previously shown that gentle saline extraction of S. aureus has revealed the presence of an extremely potent stimulator of osteoclast activation in both the murine calvarial bone resorption assay and the isolated chick osteoclast resorption assay. In order to investigate the mechanism of action of this surface-associated material (SAM), we have investigated its capacity to recruit osteoclasts.</p><p><strong>Methods: </strong>The murine bone marrow osteoclast recruitment assay was used. The ability of the recruited cells to resorb dentine slices was also investigated. Results. The SAM from S. aureus dose dependently stimulated tartrate-resistant acid phosphatase (TRAP)-positive osteoclast formation and pit formation on dentine slices. Neutralization of the cytokines tumour necrosis factor alpha and interleukin (IL)-6 totally inhibited, but antagonism of IL-1 only partially blocked, the stimulated maturation of osteoclast-like cells.</p><p><strong>Conclusion: </strong>These findings suggest that bone destruction associated with local infection by S. aureus is due to the stimulation of osteoclast formation induced by the action of the easily solubilized SAM, and could explain the large numbers of osteoclasts found in infarcted bone in osteomyelitis.</p>","PeriodicalId":9307,"journal":{"name":"British journal of rheumatology","volume":"37 10","pages":"1095-101"},"PeriodicalIF":0.0000,"publicationDate":"1998-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/rheumatology/37.10.1095","citationCount":"79","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"British journal of rheumatology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/rheumatology/37.10.1095","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 79

Abstract

Objective: Staphylococcus aureus is the cause of bone destruction in osteomyelitis, bacterial arthritis and orthopaedic implant failure. We have previously shown that gentle saline extraction of S. aureus has revealed the presence of an extremely potent stimulator of osteoclast activation in both the murine calvarial bone resorption assay and the isolated chick osteoclast resorption assay. In order to investigate the mechanism of action of this surface-associated material (SAM), we have investigated its capacity to recruit osteoclasts.

Methods: The murine bone marrow osteoclast recruitment assay was used. The ability of the recruited cells to resorb dentine slices was also investigated. Results. The SAM from S. aureus dose dependently stimulated tartrate-resistant acid phosphatase (TRAP)-positive osteoclast formation and pit formation on dentine slices. Neutralization of the cytokines tumour necrosis factor alpha and interleukin (IL)-6 totally inhibited, but antagonism of IL-1 only partially blocked, the stimulated maturation of osteoclast-like cells.

Conclusion: These findings suggest that bone destruction associated with local infection by S. aureus is due to the stimulation of osteoclast formation induced by the action of the easily solubilized SAM, and could explain the large numbers of osteoclasts found in infarcted bone in osteomyelitis.

来自金黄色葡萄球菌的表面相关蛋白刺激破骨细胞发生:在金黄色葡萄球菌诱导的骨病理中的可能作用。
目的:金黄色葡萄球菌是骨髓炎、细菌性关节炎和骨科植入物失败中导致骨破坏的原因。我们之前的研究表明,在小鼠颅骨骨吸收实验和分离的鸡破骨细胞吸收实验中,金黄色葡萄球菌的温和盐水提取显示出一种非常有效的破骨细胞激活刺激物的存在。为了研究这种表面相关材料(SAM)的作用机制,我们研究了它招募破骨细胞的能力。方法:采用小鼠骨髓破骨细胞募集法。我们还研究了再生细胞对牙本质切片的吸收能力。结果。来自金黄色葡萄球菌的SAM剂量依赖性地刺激了牙本质切片上酒石酸抗性酸性磷酸酶(TRAP)阳性的破骨细胞的形成和坑的形成。细胞因子肿瘤坏死因子和白细胞介素(IL)-6的中和作用完全抑制,但IL-1的拮抗作用仅部分阻断,刺激了破骨细胞样细胞的成熟。结论:提示金黄色葡萄球菌局部感染引起的骨破坏是由于易溶解的SAM刺激破骨细胞形成所致,这可以解释骨髓炎梗死骨中大量破骨细胞的存在。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信