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      Curcumin liposomes interfere with quorum sensing system of Aeromonas sobria and in silico analysis

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      1 , 3 , 2 , 4 , 3 , 1 ,
      Scientific Reports
      Nature Publishing Group UK

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          Abstract

          Aeromonas sobria is opportunistic pathogen frequently found in environment and food. Interfering with its quorum sensing (QS) system could be a promising way to alleviate its virulence. In this study, curcumin liposomes were prepared and their characteristics like particle size, zeta potential, PDI (Polymey Disperse Index), encapsulation efficiency and loading capacity were measured. The quorum sensing inhibitory effect of curcumin liposomes under sub-MIC (Minimum Inhibitory Concentration) on siderophore production, swimming and swarming motility, extracellular proteases, biofilm formation and AHLs (N-acylhomoserine lactones) production of A. sobria were also determined. The results showed that, the curcumin liposomes with high encapsulation capacity (84.51 ± 0.58%) were stable and homogeneous. QS-regulated phenotypes of the pathogen were significantly inhibited by curcumin liposomes. The in silico analysis revealed that the QS system of A. sobria may be inhibited by released curcumin from curcumin liposomes through interacting with the built LuxI type protein and blocking the production of AHLs.

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          Quorum sensing and Chromobacterium violaceum: exploitation of violacein production and inhibition for the detection of N-acylhomoserine lactones.

          Quorum sensing relies upon the interaction of a diffusible signal molecule with a transcriptional activator protein to couple gene expression with cell population density. In Gram-negative bacteria, such signal molecules are usually N-acylhomoserine lactones (AHLs) which differ in the structure of their N-acyl side chains. Chromobacterium violaceum, a Gram-negative bacterium commonly found in soil and water, produces the characteristic purple pigment violacein. Previously the authors described a violacein-negative, mini-Tn5 mutant of C. violaceum (CV026) in which pigment production can be restored by incubation with supernatants from the wild-type strain. To develop this mutant as a general biosensor for AHLs, the natural C. violaceum AHL molecule was first chemically characterized. By using solvent extraction, HPLC and mass spectrometry, a single AHL, N-hexanoyl-L-homoserine lactone (HHL), was identified in wild-type C. violaceum culture supernatants which was absent from CV026. Since the production of violacein constitutes a simple assay for the detection of AHLs, we explored the ability of CV026 to respond to a series of synthetic AHL and N-acylhomocysteine thiolactone (AHT) analogues. In CV026, violacein is inducible by all the AHL and AHT compounds evaluated with N-acyl side chains from C4 to C8 in length, with varying degrees of sensitivity. Although AHL compounds with N-acyl side chains from C10 to C14 are unable to induce violacein production, if an activating AHL (e.g. HHL) is incorporated into the agar, these long-chain AHLs can be detected by their ability to inhibit violacein production. The versatility of CV026 in facilitating detection of AHL mixtures extracted from culture supernatants and separated by thin-layer chromatography is also demonstrated. These simple bioassays employing CV026 thus greatly extend the ability to detect a wide spectrum of AHL signal molecules.
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            6-Gingerol reduces Pseudomonas aeruginosa biofilm formation and virulence via quorum sensing inhibition

            Pseudomonas aeruginosa is a well-known pathogenic bacterium that forms biofilms and produces virulence factors via quorum sensing (QS). Interfering with normal QS interactions between signal molecules and their cognate receptors is a developing strategy for attenuating its virulence. Here we tested the hypothesis that 6-gingerol, a pungent oil of fresh ginger, reduces biofilm formation and virulence by antagonistically binding to P. aeruginosa QS receptors. In silico studies demonstrated molecular binding occurs between 6-gingerol and the QS receptor LasR through hydrogen bonding and hydrophobic interactions. Experimentally 6-gingerol reduced biofilm formation, several virulence factors (e.g., exoprotease, rhamnolipid, and pyocyanin), and mice mortality. Further transcriptome analyses demonstrated that 6-gingerol successfully repressed QS-induced genes, specifically those related to the production of virulence factors. These results strongly support our hypothesis and offer insight into the molecular mechanism that caused QS gene repression.
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              Inhibition of Candida albicans Biofilm Formation by Farnesol, a Quorum-Sensing Molecule

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                Author and article information

                Contributors
                lijr6491@163.com
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                17 August 2017
                17 August 2017
                2017
                : 7
                : 8612
                Affiliations
                [1 ]ISNI 0000 0001 0708 1323, GRID grid.258151.a, , School of Food Science and Technology, Jiangnan University, ; Wuxi, 214122 China
                [2 ]Key Laboratory of Biotechnology and Bioresources Utilization (Dalian Minzu University), Ministry of Education, Dalian, Liaoning 116600 China
                [3 ]GRID grid.440654.7, , College of Food Science and Technology, Bohai University, Food Safety Key Lab of Liaoning Province, National & Local Joint Engineering Research Center of Storage, Processing and Safety Control Technology for Fresh Agricultural and Aquatic Products, ; Jinzhou, Liaoning 121013 China
                [4 ]ISNI 0000 0004 1755 0738, GRID grid.419102.f, , School of Chemical and Environmental Engineering, Shanghai Institute of Technology, ; Shanghai, 201418 China
                Article
                8986
                10.1038/s41598-017-08986-9
                5561023
                28819178
                ea51f45b-97a1-499c-a20a-d082be0ca542
                © The Author(s) 2017

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 21 February 2017
                : 19 July 2017
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