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种植体感染中葡萄球菌生物膜的形成。分子机制综述及其对生物膜耐药材料的影响。

Biofilm formation in Staphylococcus implant infections. A review of molecular mechanisms and implications for biofilm-resistant materials.

机构信息

Research Unit on Implant Infections, Rizzoli Orthopaedic Institute, Via di Barbiano 1/10, 40136 Bologna, Italy.

出版信息

Biomaterials. 2012 Sep;33(26):5967-82. doi: 10.1016/j.biomaterials.2012.05.031. Epub 2012 Jun 12.

DOI:10.1016/j.biomaterials.2012.05.031
PMID:22695065
Abstract

Implant infections in orthopaedics, as well as in many other medical fields, are chiefly caused by staphylococci. The ability of growing within a biofilm enhances the chances of staphylococci to protect themselves from host defences, antibiotic therapies, and biocides. Advances in scientific knowledge on structural molecules (exopolysaccharide, proteins, teichoic acids, and the most recently described extracellular DNA), on the synthesis and genetics of staphylococcal biofilms, and on the complex network of signal factors that intervene in their control are here presented, also reporting on the emerging strategies to disrupt or inhibit them. The attitude of polymorphonuclear neutrophils and macrophages to infiltrate and phagocytise biofilms, as well as the ambiguous behaviour exhibited by these innate immune cells in biofilm-related implant infections, are here discussed. Research on anti-biofilm biomaterials is focused, reviewing materials loaded with antibacterial substances, or coated with anti-adhesive/anti-bacterial immobilized agents, or surfaced with nanostructures. Latter approaches appear promising, since they avoid the spread of antibacterial substances in the neighbouring tissues with the consequent risk of inducing bacterial resistance.

摘要

骨科以及许多其他医学领域的植入物感染主要是由葡萄球菌引起的。在生物膜内生长的能力增强了葡萄球菌保护自己免受宿主防御、抗生素治疗和杀生物剂的能力。本文介绍了关于结构分子(胞外多糖、蛋白质、磷壁酸和最近描述的细胞外 DNA)、葡萄球菌生物膜合成和遗传学以及参与其调控的复杂信号因子网络的科学知识进展,还报告了破坏或抑制生物膜的新兴策略。本文讨论了多形核粒细胞和巨噬细胞浸润和吞噬生物膜的情况,以及这些先天免疫细胞在与生物膜相关的植入物感染中的表现出的模棱两可的行为。抗生物膜生物材料的研究集中在负载抗菌物质的材料上,或涂有抗粘附/抗菌固定剂,或表面具有纳米结构。后一种方法似乎很有前景,因为它们避免了抗菌物质在邻近组织中的扩散,从而降低了诱导细菌耐药性的风险。

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