Inhibition of Escherichia coli O157:H7 motility and biofilm by β-Sitosterol glucoside

Vikram, Amit; Jayaprakasha, G.K.; Uckoo, Ram M.

doi:10.1016/j.bbagen.2013.07.022

Cited by 41 publications

(30 citation statements)

References 36 publications

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“…The β‐sitosterol glucoside isolated from citrus fruit inhibited E. coli O157:H7 biofilm formation and motility by suppressing the levels of RssAB and HNS of flagellar master operon flhDC (Vikram et al . ). In a recent study, it was found that the phenolic acids (gallic acid and ferulic acid) inhibited bacterial motility of E. coli .…”

Section: Therapeuticsmentioning

confidence: 97%

“…Ginkgolic acid and Ginkgo biloba extract have shown significant inhibition of enterohaemorrhagic E. coli O157: H7 biofilm formation by downregulating curli and prophage genes (Lee et al 2014). The b-sitosterol glucoside isolated from citrus fruit inhibited E. coli O157:H7 biofilm formation and motility by suppressing the levels of RssAB and HNS of flagellar master operon flhDC (Vikram et al 2013). In a recent study, it was found that the phenolic acids (gallic acid and ferulic acid) inhibited bacterial motility of E. coli.…”

Section: Phytochemicalsmentioning

confidence: 99%

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Escherichia coli biofilm: development and therapeutic strategies

et al. 2016

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SummaryEscherichia coli biofilm consists of a bacterial colony embedded in a matrix of extracellular polymeric substances (EPS) which protects the microbes from adverse environmental conditions and results in infection. Besides being the major causative agent for recurrent urinary tract infections, E. coli biofilm is also responsible for indwelling medical device-related infectivity. The cell-tocell communication within the biofilm occurs due to quorum sensors that can modulate the key biochemical players enabling the bacteria to proliferate and intensify the resultant infections. The diversity in structural components of biofilm gets compounded due to the development of antibiotic resistance, hampering its eradication. Conventionally used antimicrobial agents have a restricted range of cellular targets and limited efficacy on biofilms. This emphasizes the need to explore the alternate therapeuticals like anti-adhesion compounds, phytochemicals, nanomaterials for effective drug delivery to restrict the growth of biofilm. The current review focuses on various aspects of E. coli biofilm development and the possible therapeutic approaches for prevention and treatment of biofilm-related infections.

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Section: Therapeuticsmentioning

confidence: 97%

Section: Phytochemicalsmentioning

confidence: 99%

Escherichia coli biofilm: development and therapeutic strategies

et al. 2016

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“…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. This inhibition probably occurs through repression of rssAB and hns, regulatory elements of the flagellar operon (Vikram et al, 2013). Essential oils from cassia (Cinnamomum aromaticum) and Peru balsam (Myroxylon balsamum) kill plant and human pathogens within biofilms in similar efficacy as the planktonic cells, and the oil of red thyme (Thymus vulgaris) is even more effective against biofilms cells than planktonic bacteria (Kavanaugh and Ribbeck, 2012).…”

Section: S Typhimuriummentioning

confidence: 99%

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

Yaron

Römling

2014

Microbial Biotechnology

220

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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“…However, traditional antimicrobial agents primarily designed to inhibit cell growth often result in bacterial drug resistance, and thus, essential oils have been studied using other developmental approaches, such as, the inhibition of biofilm formation, toxin production, bacterial quorum sensing, and of adhesive factors. For example, carvacrol and eugenol14, grapefruit limonoids15, β -sitosterol glucoside from clementine peel16, ginkgolic acids from Ginkgo biloba 17, and cinnamaldehyde and eugenol from cinnamon bark oil18, which are found in essential oils, have been reported to inhibit EHEC biofilm formation. However, few studies have been undertaken to compare the antibiofilm characteristics of large numbers of essential oils.…”

mentioning

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

157

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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Inhibition of Escherichia coli O157:H7 motility and biofilm by β-Sitosterol glucoside

Cited by 41 publications

References 36 publications

Escherichia coli biofilm: development and therapeutic strategies

Escherichia coli biofilm: development and therapeutic strategies

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

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

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