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葡萄球菌生物膜与骨之间的相互作用:生物膜的存在如何促进假体松动?

Interaction Between Staphylococcal Biofilm and Bone: How Does the Presence of Biofilm Promote Prosthesis Loosening?

作者信息

Josse Jérôme, Valour Florent, Maali Yousef, Diot Alan, Batailler Cécile, Ferry Tristan, Laurent Frédéric

机构信息

CIRI - Centre International de Recherche en Infectiologie, Inserm U1111, CNRS UMR5308, ENS Lyon, Université Claude Bernard Lyon 1, Lyon, France.

Université Claude Bernard Lyon 1, Université de Lyon, Lyon, France.

出版信息

Front Microbiol. 2019 Jul 17;10:1602. doi: 10.3389/fmicb.2019.01602. eCollection 2019.

Abstract

With the aging of population, the number of indications for total joint replacement is continuously increasing. However, prosthesis loosening can happen and is related to two major mechanisms: (1) aseptic loosening due to prosthesis micromotion and/or corrosion and release of wear particles from the different components of the implanted material and (2) septic loosening due to chronic prosthetic joint infection (PJI). The "aseptic" character of prosthesis loosening has been challenged over the years, especially considering that bacteria can persist in biofilms and be overlooked during diagnosis. Histological studies on periprosthetic tissue samples reported that macrophages are the principle cells associated with aseptic loosening due to wear debris. They produce cytokines and favor an inflammatory environment that induces formation and activation of osteoclasts, leading to bone resorption and periprosthetic osteolysis. In PJIs, the presence of infiltrates of polymorphonuclear neutrophils is a major criterion for histological diagnosis. Neutrophils are colocalized with osteoclasts and zones of osteolysis. A similar inflammatory environment also develops, leading to bone resorption through osteoclasts. , , and are the main staphylococci observed in PJIs. They share the common feature to form biofilm. For and , the interaction between biofilm and immunes cells (macrophages and polymorphonuclear neutrophils) differs regarding the species. Indeed, the composition of extracellular matrix of biofilm seems to impact the interaction with immune cells. Recent papers also reported the major role of myeloid-derived suppressor cells in biofilm-associated PJIs with . These cells prevent lymphocyte infiltration and facilitate biofilm persistence. Moreover, the role of T lymphocytes is still unclear and potentially underestimates. In this review, after introducing the cellular mechanism of aseptic and septic loosening, we will focus on the interrelationships between staphylococcal biofilm, immune cells, and bone cells.

摘要

随着人口老龄化,全关节置换的适应症数量不断增加。然而,假体松动可能会发生,并且与两个主要机制有关:(1)由于假体微动和/或腐蚀以及植入材料不同部件磨损颗粒的释放导致的无菌性松动,以及(2)由于慢性人工关节感染(PJI)导致的感染性松动。多年来,假体松动的“无菌”特性受到了挑战,特别是考虑到细菌可以在生物膜中持续存在并且在诊断过程中被忽视。对假体周围组织样本的组织学研究报告称,巨噬细胞是与磨损碎片导致的无菌性松动相关的主要细胞。它们产生细胞因子并促进炎症环境,诱导破骨细胞的形成和激活,导致骨吸收和假体周围骨溶解。在PJI中,多形核中性粒细胞浸润的存在是组织学诊断的主要标准。中性粒细胞与破骨细胞和骨溶解区域共定位。类似的炎症环境也会发展,通过破骨细胞导致骨吸收。金黄色葡萄球菌、表皮葡萄球菌和溶血葡萄球菌是PJI中观察到的主要葡萄球菌。它们具有形成生物膜的共同特征。对于金黄色葡萄球菌和表皮葡萄球菌,生物膜与免疫细胞(巨噬细胞和多形核中性粒细胞)之间的相互作用因菌种而异。事实上,生物膜细胞外基质的组成似乎会影响与免疫细胞的相互作用。最近的论文还报道了髓系来源的抑制细胞在与金黄色葡萄球菌相关的PJI中的主要作用。这些细胞阻止淋巴细胞浸润并促进生物膜持续存在。此外,T淋巴细胞的作用仍不清楚且可能被低估。在这篇综述中,在介绍了无菌性和感染性松动的细胞机制后,我们将重点关注葡萄球菌生物膜、免疫细胞和骨细胞之间的相互关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0848/6653651/1aba3d40937c/fmicb-10-01602-g001.jpg

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