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本文引用的文献

1
Infectious Dose Dictates the Host Response during Staphylococcus aureus Orthopedic-Implant Biofilm Infection.感染剂量决定金黄色葡萄球菌骨科植入物生物膜感染期间的宿主反应。
Infect Immun. 2016 Jun 23;84(7):1957-1965. doi: 10.1128/IAI.00117-16. Print 2016 Jul.
2
Staphylococcus aureus Biofilms Induce Macrophage Dysfunction Through Leukocidin AB and Alpha-Toxin.金黄色葡萄球菌生物膜通过杀白细胞素AB和α毒素诱导巨噬细胞功能障碍。
mBio. 2015 Aug 25;6(4):e01021-15. doi: 10.1128/mBio.01021-15.
3
Interleukin-10 production by myeloid-derived suppressor cells contributes to bacterial persistence during Staphylococcus aureus orthopedic biofilm infection.骨髓来源的抑制性细胞产生白细胞介素-10有助于金黄色葡萄球菌骨科生物膜感染期间细菌的持续存在。
J Leukoc Biol. 2015 Dec;98(6):1003-13. doi: 10.1189/jlb.4VMA0315-125RR. Epub 2015 Jul 31.
4
IL-12 promotes myeloid-derived suppressor cell recruitment and bacterial persistence during Staphylococcus aureus orthopedic implant infection.白细胞介素-12在金黄色葡萄球菌骨科植入物感染期间促进髓源性抑制细胞募集和细菌持续存在。
J Immunol. 2015 Apr 15;194(8):3861-3872. doi: 10.4049/jimmunol.1402689. Epub 2015 Mar 11.
5
Structural basis of Staphylococcus epidermidis biofilm formation: mechanisms and molecular interactions.表皮葡萄球菌生物膜形成的结构基础:机制与分子相互作用
Front Cell Infect Microbiol. 2015 Feb 17;5:14. doi: 10.3389/fcimb.2015.00014. eCollection 2015.
6
A major role for myeloid-derived suppressor cells and a minor role for regulatory T cells in immunosuppression during Staphylococcus aureus infection.骨髓来源的抑制性细胞在金黄色葡萄球菌感染期间的免疫抑制中起主要作用,而调节性T细胞起次要作用。
J Immunol. 2015 Feb 1;194(3):1100-11. doi: 10.4049/jimmunol.1400196. Epub 2014 Dec 29.
7
Cutaneous innate immune sensing of Toll-like receptor 2-6 ligands suppresses T cell immunity by inducing myeloid-derived suppressor cells.皮肤固有免疫对 Toll 样受体 2-6 配体的感应通过诱导髓系来源的抑制细胞来抑制 T 细胞免疫。
Immunity. 2014 Nov 20;41(5):762-75. doi: 10.1016/j.immuni.2014.10.009. Epub 2014 Nov 13.
8
Temporal and stochastic control of Staphylococcus aureus biofilm development.金黄色葡萄球菌生物膜形成的时间和随机控制
mBio. 2014 Oct 14;5(5):e01341-14. doi: 10.1128/mBio.01341-14.
9
Prosthetic joint infection.人工关节感染
Clin Microbiol Rev. 2014 Apr;27(2):302-45. doi: 10.1128/CMR.00111-13.
10
The M1 and M2 paradigm of macrophage activation: time for reassessment.巨噬细胞活化的M1和M2范式:是时候重新评估了。
F1000Prime Rep. 2014 Mar 3;6:13. doi: 10.12703/P6-13. eCollection 2014.

人工关节感染期间的葡萄球菌生物膜与免疫极化

Staphylococcal Biofilms and Immune Polarization During Prosthetic Joint Infection.

作者信息

Gries Casey M, Kielian Tammy

机构信息

From the University of Nebraska, Omaha, Nebraska.

出版信息

J Am Acad Orthop Surg. 2017 Feb;25 Suppl 1(Suppl 1):S20-S24. doi: 10.5435/JAAOS-D-16-00636.

DOI:10.5435/JAAOS-D-16-00636
PMID:27922945
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5640443/
Abstract

Staphylococcal species are a leading cause of community- and nosocomial-acquired infections, where the placement of foreign materials increases infection risk. Indwelling medical devices and prosthetic implants are targets for staphylococcal cell adherence and biofilm formation. Biofilm products actively suppress proinflammatory microbicidal responses, as evident by macrophage polarization toward an anti-inflammatory phenotype and the recruitment of myeloid-derived suppressor cells. With the rise in prosthetic hip and knee arthroplasty procedures, together with the recalcitrance of biofilm infections to antibiotic therapy, it is imperative to better understand the mechanism of crosstalk between biofilm-associated bacteria and host immune cells. This review describes the current understanding of how staphylococcal biofilms evade immune-mediated clearance to establish persistent infections. The findings described herein may facilitate the identification of novel treatments for these devastating biofilm-mediated infections.

摘要

葡萄球菌属是社区获得性感染和医院获得性感染的主要病因,在这种情况下,异物的植入会增加感染风险。留置医疗设备和假体植入物是葡萄球菌细胞黏附和生物膜形成的目标。生物膜产物会积极抑制促炎杀菌反应,巨噬细胞向抗炎表型极化以及髓源性抑制细胞的募集就证明了这一点。随着人工髋关节和膝关节置换手术的增加,以及生物膜感染对抗生素治疗的顽固性,更好地了解生物膜相关细菌与宿主免疫细胞之间的串扰机制势在必行。本综述描述了目前对葡萄球菌生物膜如何逃避免疫介导的清除以建立持续性感染的理解。本文所述的研究结果可能有助于确定针对这些毁灭性生物膜介导感染的新疗法。