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Curr Protoc Microbiol. 2005 Jul;Chapter 1:Unit 1B.1. doi: 10.1002/9780471729259.mc01b01s00.
2
Biomaterial strategies to reduce implant-associated infections.减少植入物相关感染的生物材料策略。
Int J Artif Organs. 2007 Sep;30(9):828-41. doi: 10.1177/039139880703000913.
3
BifA, a cyclic-Di-GMP phosphodiesterase, inversely regulates biofilm formation and swarming motility by Pseudomonas aeruginosa PA14.双功能A(BifA)是一种环二鸟苷酸磷酸二酯酶,它对铜绿假单胞菌PA14的生物膜形成和群体运动起反向调节作用。
J Bacteriol. 2007 Nov;189(22):8165-78. doi: 10.1128/JB.00586-07. Epub 2007 Jun 22.
4
The challenge of treating biofilm-associated bacterial infections.治疗生物膜相关细菌感染的挑战。
Clin Pharmacol Ther. 2007 Aug;82(2):204-9. doi: 10.1038/sj.clpt.6100247. Epub 2007 May 30.
5
Physiological aspects. Part 1 in a series of papers devoted to surfactants in microbiology and biotechnology.生理学方面。关于微生物学和生物技术中表面活性剂的系列论文的第1部分。
Biotechnol Adv. 2006 Nov-Dec;24(6):604-20. doi: 10.1016/j.biotechadv.2006.08.001. Epub 2006 Aug 9.
6
Saccharomyces cerevisiae-based molecular tool kit for manipulation of genes from gram-negative bacteria.用于操作革兰氏阴性菌基因的基于酿酒酵母的分子工具包。
Appl Environ Microbiol. 2006 Jul;72(7):5027-36. doi: 10.1128/AEM.00682-06.
7
Comblike poly(ethylene oxide)/hydrophobic C6 branched chitosan surfactant polymers as anti-infection surface modifying agents.梳状聚环氧乙烷/疏水性C6支链壳聚糖表面活性剂聚合物作为抗感染表面改性剂。
Colloids Surf B Biointerfaces. 2006 May 1;49(2):117-25. doi: 10.1016/j.colsurfb.2006.03.007. Epub 2006 Apr 18.
8
An ordered, nonredundant library of Pseudomonas aeruginosa strain PA14 transposon insertion mutants.铜绿假单胞菌PA14菌株转座子插入突变体的有序、非冗余文库。
Proc Natl Acad Sci U S A. 2006 Feb 21;103(8):2833-8. doi: 10.1073/pnas.0511100103. Epub 2006 Feb 13.
9
Biosurfactants: potential applications in medicine.生物表面活性剂:在医学中的潜在应用。
J Antimicrob Chemother. 2006 Apr;57(4):609-18. doi: 10.1093/jac/dkl024. Epub 2006 Feb 9.
10
A three-component regulatory system regulates biofilm maturation and type III secretion in Pseudomonas aeruginosa.一种三组分调节系统调控铜绿假单胞菌中的生物膜成熟和III型分泌。
J Bacteriol. 2005 Feb;187(4):1441-54. doi: 10.1128/JB.187.4.1441-1454.2005.

聚山梨醇酯80对铜绿假单胞菌生物膜形成的抑制作用及其被分泌的脂肪酶LipA的裂解作用。

Polysorbate 80 inhibition of Pseudomonas aeruginosa biofilm formation and its cleavage by the secreted lipase LipA.

作者信息

Toutain-Kidd Christine M, Kadivar Samoneh C, Bramante Carolyn T, Bobin Stephen A, Zegans Michael E

机构信息

Department of Surgery, Dartmouth Medical School, Hanover, New Hampshire 03755, USA.

出版信息

Antimicrob Agents Chemother. 2009 Jan;53(1):136-45. doi: 10.1128/AAC.00500-08. Epub 2008 Oct 27.

DOI:10.1128/AAC.00500-08
PMID:18955535
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2612155/
Abstract

Surface-associated bacterial communities known as biofilms are an important source of nosocomial infections. Microorganisms such as Pseudomonas aeruginosa can colonize the abiotic surfaces of medical implants, leading to chronic infections that are difficult to eradicate. Our study demonstrates that polysorbate 80 (PS80), a surfactant commonly added to food and medicines, is able to inhibit biofilm formation by P. aeruginosa on a variety of surfaces, including contact lenses. Many clinical isolates of P. aeruginosa, as well as gram-negative and gram-positive clinical isolates, were also inhibited in their ability to form biofilms in the presence of PS80. A P. aeruginosa mutant able to form biofilms in the presence of this surfactant was identified and characterized, and it was revealed that this mutant overexpresses a lipase, LipA. Surfactants such as PS80 can be cleaved by lipases, and we demonstrate that PS80 is cleaved by LipA at its ester bond. Finally, polyethoxylated(20) oleyl alcohol, a chemical with a structure that is similar to that of PS80 but that lacks the ester bond of PS80, can inhibit the biofilm formation of P. aeruginosa strains, including the mutant overexpressing LipA. Our results demonstrate that surfactants such as PS80 can inhibit bacterial biofilm formation on medically relevant materials at concentrations demonstrated to be safe in humans and suggest that the understanding of the mechanisms of bacterial resistance to such surfactants will be important in developing clinically effective derivatives.

摘要

被称为生物膜的表面相关细菌群落是医院感染的重要来源。诸如铜绿假单胞菌等微生物能够在医疗植入物的非生物表面定殖,导致难以根除的慢性感染。我们的研究表明,聚山梨醇酯80(PS80),一种通常添加到食品和药品中的表面活性剂,能够抑制铜绿假单胞菌在包括隐形眼镜在内的各种表面形成生物膜。许多铜绿假单胞菌临床分离株以及革兰氏阴性和革兰氏阳性临床分离株在PS80存在下形成生物膜的能力也受到抑制。鉴定并表征了一种在这种表面活性剂存在下能够形成生物膜的铜绿假单胞菌突变体,结果表明该突变体过表达一种脂肪酶LipA。诸如PS80之类的表面活性剂可被脂肪酶裂解,并且我们证明PS80在其酯键处被LipA裂解。最后,聚乙氧基化(20)油醇,一种结构与PS80相似但缺乏PS80酯键的化学物质,能够抑制包括过表达LipA的突变体在内的铜绿假单胞菌菌株的生物膜形成。我们的结果表明,诸如PS80之类的表面活性剂能够在已证明对人类安全的浓度下抑制医学相关材料上的细菌生物膜形成,并表明了解细菌对此类表面活性剂的耐药机制对于开发临床有效的衍生物将具有重要意义。