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肉桂醛破坏铜绿假单胞菌的生物膜形成和群体运动。

Cinnamaldehyde disrupts biofilm formation and swarming motility of Pseudomonas aeruginosa.

作者信息

Topa Sanjida Halim, Subramoni Sujatha, Palombo Enzo A, Kingshott Peter, Rice Scott A, Blackall Linda L

机构信息

1​Department of Chemistry and Biotechnology, School of Science, Swinburne University of Technology, Hawthorn, Victoria, Australia.

2​Singapore Centre for Environmental Life Sciences Engineering (SCELSE), Nanyang Technological University, Nanyang Avenue, Singapore.

出版信息

Microbiology (Reading). 2018 Sep;164(9):1087-1097. doi: 10.1099/mic.0.000692. Epub 2018 Jul 12.

Abstract

Bacterial biofilms can cause serious health care complications associated with increased morbidity and mortality. There is an urge to discover and develop new biofilm inhibitors from natural products or by modifying natural compounds or understanding the modes of action of existing compounds. Cinnamaldehyde (CAD), one of the major components of cinnamon oil, has been demonstrated to act as an antimicrobial agent against a number of Gram-negative and Gram-positive pathogens, including Pseudomonas aeruginosa, Helicobacter pylori and Listeria monocytogenes. Despite the mechanism of action of CAD against the model organism P. aeruginosa being undefined, based on its antimicrobial properties, we hypothesized that it may disrupt preformed biofilms of P. aeruginosa. The minimum inhibitory concentration (MIC) of CAD for planktonic P. aeruginosa was determined to be 11.8 mM. Membrane depolarization assays demonstrated disruption of the transmembrane potential of P. aeruginosa. CAD at 5.9 mM (0.5 MIC) disrupted preformed biofilms by 75.6 % and 3 mM CAD (0.25 MIC) reduced the intracellular concentrations of the secondary messenger, bis-(3'-5')-cyclic dimeric guanosine monophosphate (c-di-GMP), which controls P. aeruginosa biofilm formation. The swarming motility of P. aeruginosa was also reduced by CAD in a concentration-dependent manner. Collectively, these findings show that sub-MICs of CAD can disrupt biofilms and other surface colonization phenotypes through the modulation of intracellular signalling processes.

摘要

细菌生物膜可导致严重的医疗保健并发症,与发病率和死亡率增加相关。迫切需要从天然产物中发现和开发新的生物膜抑制剂,或通过修饰天然化合物或了解现有化合物的作用模式来实现。肉桂醛(CAD)是肉桂油的主要成分之一,已被证明可作为一种抗菌剂,对抗多种革兰氏阴性和革兰氏阳性病原体,包括铜绿假单胞菌、幽门螺杆菌和单核细胞增生李斯特菌。尽管CAD对模式生物铜绿假单胞菌的作用机制尚不清楚,但基于其抗菌特性,我们推测它可能破坏铜绿假单胞菌预先形成的生物膜。CAD对浮游铜绿假单胞菌的最低抑菌浓度(MIC)测定为11.8 mM。膜去极化试验表明铜绿假单胞菌的跨膜电位受到破坏。5.9 mM(0.5 MIC)的CAD可破坏预先形成的生物膜75.6%,3 mM CAD(0.25 MIC)可降低控制铜绿假单胞菌生物膜形成的第二信使双(3'-5')-环二聚鸟苷单磷酸(c-di-GMP)的细胞内浓度。CAD还以浓度依赖的方式降低了铜绿假单胞菌的群体运动性。总的来说,这些发现表明,CAD的亚MIC浓度可通过调节细胞内信号传导过程来破坏生物膜和其他表面定植表型。

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