Inhibition of Pseudomonas aeruginosa and Escherichia coli O157:H7 Biofilm Formation by Plant Metabolite ε-Viniferin

Capsicum peppers have not been investigated as sources of quorum sensing (QS) inhibitors. This study aimed to identify compounds in pimenta‐malagueta (Capsicum frutescens) and red pepper (Capsicum annuum) extracts and to evaluate their effect on violacein production in Chromobacterium violaceum ATCC 12472 and C. violaceum CV026, as well as biofilm formation (BF) in Pseudomonas aeruginosa PAO1 and Serratia marcescens MG1. Among the extracts, pimenta‐malagueta methanolic extract (PMME) was chosen because it contained capsaicin, dihydrocapsaicin, and luteolin in greater amount than the other extracts. In general, PMME partially inhibited bacterial growth at 2.5 and 5.0 mg/mL, as well as capsaicin at 100 µg/mL and luteolin at 62.5, 125, and 250 µg/mL. At lower concentrations, PMME and luteolin reduced violacein production in C. violaceum ATCC 12472 without affecting growth, a result that was not observed with capsaicin. We show that violacein inhibition by PMME is likely due to luteolin. In silico docking evaluation showed that luteolin binds to the CviR QS regulator. Crystal violet staining and confocal microscopy revealed that BF was increased by PMME and capsaicin, being remarkably superior for P. aeruginosa PAO1 at 30 °C. Capsaicin is not an effective QS inhibitor, while luteolin should be further investigated for its potential effects in QS regulated phenotypes. Practical Application Quorum sensing (QS) is a form of bacterial communication targeted for studies aiming to inhibit bacterial virulence. QS regulates phenotypes that influence microbial activities across many areas, including Food Science. Capsicum frutescens is a type of chili pepper consumed in Brazil, rich in bioactive compounds such as capsaicin (which gives its pungency) and luteolin (a phenolic compound). We show that C. frutescens extract and luteolin inhibit QS in a model bacterium, along with the possible molecular mechanism of inhibition. Capsaicin did not inhibit QS neither biofilm formation. Luteolin should be further investigated for its QS inhibition properties and biotechnological applications.

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“…Similar effects were reported by Cho et al. () evaluating some flavonoids on BF by P. aeruginosa PA14. Plyuta et al.…”

Section: Resultssupporting

confidence: 89%

Effect of Capsicum Frutescens Extract, Capsaicin, and Luteolin on Quorum Sensing Regulated Phenotypes

Rivera

Hassimotto

Bueris

et al. 2019

Journal of Food Science

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“…EHEC strains contain a series of fimbriae such as curli fimbriae (Csg), type I fimbriae (Fim), E. coli common pilus (Ecp), F9 fimbriae (Z2200), and other fimbrial proteins29. It has been also reported that several phytochemicals, such as, 3-indolylacetonitrile30, phloretin31, resveratrol (and its dimer viniferin)3233, cinnamaldehyde18, coumarin34, and ginkgolic acids17 inhibit EHEC biofilm formation primarily by inhibiting curli fimbriae production. Hence, it appears that fimbriae-reducing ability is not rare in the plant kingdom and that the fimbriae inhibition could be viewed a practical target for suppressing EHEC biofilm formation.…”

Section: Discussionmentioning

confidence: 99%

Essential Oils and Eugenols Inhibit Biofilm Formation and the Virulence of Escherichia coli O157:H7

Kim

Lee

Gwon

et al. 2016

Sci Rep

Self Cite

153

103

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Enterohemorrhagic Escherichia coli O157:H7 (EHEC) has caused foodborne outbreaks worldwide and the bacterium forms antimicrobial-tolerant biofilms. We investigated the abilities of various plant essential oils and their components to inhibit biofilm formation by EHEC. Bay, clove, pimento berry oils and their major common constituent eugenol at 0.005% (v/v) were found to markedly inhibit EHEC biofilm formation without affecting planktonic cell growth. In addition, three other eugenol derivatives isoeugenol, 2-methoxy-4-propylphenol, and 4-ethylguaiacol had antibiofilm activity, indicating that the C-1 hydroxyl unit, the C-2 methoxy unit, and C-4 alkyl or alkane chain on the benzene ring of eugenol play important roles in antibiofilm activity. Interestingly, these essential oils and eugenol did not inhibit biofilm formation by three laboratory E. coli K-12 strains that reduced curli fimbriae production. Transcriptional analysis showed that eugenol down-regulated 17 of 28 genes analysed, including curli genes (csgABDFG), type I fimbriae genes (fimCDH) and ler-controlled toxin genes (espD, escJ, escR, and tir), which are required for biofilm formation and the attachment and effacement phenotype. In addition, biocompatible poly(lactic-co-glycolic acid) coatings containing clove oil or eugenol exhibited efficient biofilm inhibition on solid surfaces. In a Caenorhabditis elegans nematode model, clove oil and eugenol attenuated the virulence of EHEC.

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“…In another study, Carex plant extracts inhibited E. coli O157:H7 and Pseudomonas aeruginosa biofilm formation without affecting planktonic cells growth. One of the active antibiofilm compounds in these extracts was ε‐viniferin (Cho et al ., ). Plant sterols such as the β‐sitosterol glucoside from citrus are potent inhibitors of E. coli O157:H7 biofilm formation and motility, without affecting the cell viability.…”

Section: The Plant Response and Its Effect On Bacterial Biofilmsmentioning

confidence: 97%

Biofilm formation by enteric pathogens and its role in plant colonization and persistence

Yaron

Römling

2014

Microbial Biotechnology

211

144

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The significant increase in foodborne outbreaks caused by contaminated fresh produce, such as alfalfa sprouts, lettuce, melons, tomatoes and spinach, during the last 30 years stimulated investigation of the mechanisms of persistence of human pathogens on plants. Emerging evidence suggests that Salmonella enterica and Escherichia coli, which cause the vast majority of fresh produce outbreaks, are able to adhere to and to form biofilms on plants leading to persistence and resistance to disinfection treatments, which subsequently can cause human infections and major outbreaks. In this review, we present the current knowledge about host, bacterial and environmental factors that affect the attachment to plant tissue and the process of biofilm formation by S. enterica and E. coli, and discuss how biofilm formation assists in persistence of pathogens on the plants. Mechanisms used by S. enterica and E. coli to adhere and persist on abiotic surfaces and mammalian cells are partially similar and also used by plant pathogens and symbionts. For example, amyloid curli fimbriae, part of the extracellular matrix of biofilms, frequently contribute to adherence and are upregulated upon adherence and colonization of plant material. Also the major exopolysaccharide of the biofilm matrix, cellulose, is an adherence factor not only of S. enterica and E. coli, but also of plant symbionts and pathogens. Plants, on the other hand, respond to colonization by enteric pathogens with a variety of defence mechanisms, some of which can effectively inhibit biofilm formation. Consequently, plant compounds might be investigated for promising novel antibiofilm strategies.

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Inhibition of Pseudomonas aeruginosa and Escherichia coli O157:H7 Biofilm Formation by Plant Metabolite ε-Viniferin

Cited by 89 publications

References 43 publications

Effect of Capsicum Frutescens Extract, Capsaicin, and Luteolin on Quorum Sensing Regulated Phenotypes

Effect of Capsicum Frutescens Extract, Capsaicin, and Luteolin on Quorum Sensing Regulated Phenotypes

Essential Oils and Eugenols Inhibit Biofilm Formation and the Virulence of Escherichia coli O157:H7

Biofilm formation by enteric pathogens and its role in plant colonization and persistence

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