Halogenated furanones from the red alga, Delisea pulchra, inhibit carbapenem antibiotic synthesis and exoenzyme virulence factor production in the phytopathogen Erwinia carotovora

Manefield, M

doi:10.1016/s0378-1097(01)00460-8

Cited by 57 publications

(68 citation statements)

References 20 publications

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“…Similar results could be seen in treating Brachionus rotifer aquaculture infected with V. harveyi (246), and treatment of V. anguillarum infections with furanone in rainbow trout delayed mortality by several days (242). The ability of the plant pathogen Erwinia carotovora to produce carbapenem antibiotics was found to be disrupted when grown in the presence of furanone, and the compound slightly decreased protease and cellulase activities (249).…”

Section: Natural-product Qs Inhibitorssupporting

confidence: 62%

Exploiting Quorum Sensing To Confuse Bacterial Pathogens

LaSarre

Federle

2013

Microbiol Mol Biol Rev

677

556

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SUMMARY Cell-cell communication, or quorum sensing, is a widespread phenomenon in bacteria that is used to coordinate gene expression among local populations. Its use by bacterial pathogens to regulate genes that promote invasion, defense, and spread has been particularly well documented. With the ongoing emergence of antibiotic-resistant pathogens, there is a current need for development of alternative therapeutic strategies. An antivirulence approach by which quorum sensing is impeded has caught on as a viable means to manipulate bacterial processes, especially pathogenic traits that are harmful to human and animal health and agricultural productivity. The identification and development of chemical compounds and enzymes that facilitate quorum-sensing inhibition (QSI) by targeting signaling molecules, signal biogenesis, or signal detection are reviewed here. Overall, the evidence suggests that QSI therapy may be efficacious against some, but not necessarily all, bacterial pathogens, and several failures and ongoing concerns that may steer future studies in productive directions are discussed. Nevertheless, various QSI successes have rightfully perpetuated excitement surrounding new potential therapies, and this review highlights promising QSI leads in disrupting pathogenesis in both plants and animals.

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Section: Natural-product Qs Inhibitorssupporting

confidence: 62%

Exploiting Quorum Sensing To Confuse Bacterial Pathogens

LaSarre

Federle

2013

Microbiol Mol Biol Rev

677

556

View full text Add to dashboard Cite

show abstract

“…Inhibition of QS circuits by QS antagonists, such as the halogenated furanones from the redsea alga Delisea pulchra, offers an attractive method for inhibiting bacterial pathogens. [26][27][28][29][30][31][32][33][34][35][36] B. anthracis synthesizes AI-2 or an AI-2-like auto-inducer molecule that induces bioluminescence in the Vibrio harveyi Quorum-sensing (Qs), the regulation of bacterial gene expression in response to changes in cell density, involves pathways that synthesize signaling molecules (auto-inducers). The luxS/AI-2-mediated QS system has been identified in both Grampositive and Gram-negative bacteria.…”

Section: Introductionmentioning

confidence: 99%

Role ofluxSinBacillus anthracisgrowth and virulence factor expression

Jones¹,

Peterson²,

Benn³

et al. 2010

Virulence

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“…Studies of the interactions between halogenated furanones and LuxR homologues have focused on LuxR from V. fischeri (Manefield et al, 1999(Manefield et al, , 2002 but halogenated furanones also inhibit quorum-sensing-controlled phenotypes in Serratia liquefaciens (Givskov et al, 1996), V. harveyi (Manefield et al, 2000), Erwinia carotovora (Manefield et al, 2001) and Chromobacterium violaceum (Martinelli et al, 2004). Despite functional promiscuity, the natural furanones showed a limited effect on a LasR-controlled AHL biosensor .…”

Section: Initial Model For the Molecular Interaction Between Luxr Andmentioning

confidence: 99%

The LuxR receptor: the sites of interaction with quorum-sensing signals and inhibitors

Koch

Liljefors

Persson³

et al. 2005

Microbiology

147

103

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The function of LuxR homologues as quorum sensors is mediated by the binding of N-acyl-l-homoserine lactone (AHL) signal molecules to the N-terminal receptor site of the proteins. In this study, site-directed mutagenesis was carried out of the amino acid residues comprising the receptor site of LuxR from Vibrio fischeri, and the ability of the L42A, L42S, Y62F, W66F, D79N, W94D, V109D, V109T and M135A LuxR mutant proteins to activate green fluorescent protein expression from a PluxI promoter was measured. X-ray crystallographic studies of the LuxR homologue TraR indicated that residues Y53 and W57 form hydrogen bonds to the 1-carbonyl group and the ring carbonyl group, respectively, of the cognate AHL signal. Based on the activity and signal specificity of the LuxR mutant proteins, and on molecular modelling, a model is suggested in which Y62 (corresponding to Y53 in TraR) forms a hydrogen bond with the ring carbonyl group rather than the 1-carbonyl group, while W66 (corresponding to W57 in TraR) forms a hydrogen bond to the 1-carbonyl group. This flips the position of the acyl side chain in the LuxR/signal molecule complex compared to the TraR/signal molecule complex. Halogenated furanones from the marine alga Delisea pulchra and the synthetic signal analogue N-(sulfanylacetyl)-l-homoserine lactone can block quorum sensing. The LuxR mutant proteins were insensitive to inhibition by N-(propylsulfanylacetyl)-l-homoserine lactone. In contrast, the mutations had only a minor effect on the sensitivity of the proteins to halogenated furanones, and the data strongly suggest that these compounds do not compete in a ‘classic’ way with N-3-oxohexanoyl-l-homoserine lactone for the binding site. Based on modelling and experimental data it is suggested that these compounds bind in a non-agonist fashion.

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Halogenated furanones from the red alga, Delisea pulchra, inhibit carbapenem antibiotic synthesis and exoenzyme virulence factor production in the phytopathogen Erwinia carotovora

Cited by 57 publications

References 20 publications

Exploiting Quorum Sensing To Confuse Bacterial Pathogens

Exploiting Quorum Sensing To Confuse Bacterial Pathogens

Role ofluxSinBacillus anthracisgrowth and virulence factor expression

The LuxR receptor: the sites of interaction with quorum-sensing signals and inhibitors

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