表皮葡萄球菌假体关节感染的发病机制:细菌在成骨细胞、滑膜细胞和内皮细胞中的粘附和内化。

IF 2
Anne Lise Maucotel, Deborah M Crepin, Allison Faure, Florent Valour, Frédéric Laurent, Jérôme Josse
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引用次数: 0

摘要

表皮葡萄球菌在假体关节感染(PJIs)中经常被分离出来。与金黄色葡萄球菌不同,其在细胞内的内化和持久性存在争议。我们的目的是确定内化是否参与表皮葡萄球菌PJIs的病理生理。利用体外模型研究了表皮葡萄球菌PJI分离株的粘附和内化。尽管与金黄色葡萄球菌SH1000参考菌株的粘附水平相似,但表皮葡萄球菌分离株在成骨细胞、滑膜细胞和内皮细胞中的内化程度较低。表皮葡萄球菌的内化依赖于菌株和细胞类型。我们的研究结果不支持表皮葡萄球菌内化是PJIs的关键因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pathogenesis of Staphylococcus epidermidis prosthetic joint infections: bacterial adhesion and internalization in osteoblasts, synoviocytes and endothelial cells.

Staphylococcus epidermidis is frequently isolated during prosthetic joint infections (PJIs). Unlike Staphylococcus aureus, its internalization and persistence within cells are controversial. We aimed to determine whether internalization is involved in the pathophysiology of S. epidermidis PJIs. Adhesion and internalization of S. epidermidis PJI isolates have been studied using an in vitro model. Despite similar adhesion levels to the S. aureus SH1000 reference strain, S. epidermidis isolates had a low internalization in osteoblasts, synoviocytes and endothelial cells. Internalization of S. epidermidis is strain- and cell-type dependent. Our results do not support S. epidermidis internalization as a key factor in PJIs.

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