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

Abstract

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.

Antivirulence properties and related mechanisms of spice essential oils: A comprehensive review

“…Spice essential oils have been reported to interfere with biofilm formation of different bacteria at sub‐MICs under in vitro conditions, without evidently affecting the growth and metabolic activities of bacteria. For instance, essential oils from oregano, clove, thyme, turmeric, garlic, lemon, and their major bioactive compounds, such as carvacrol, eugenol, thymol, curcumin, allicin, and limonene, show high biofilm inhibition activities (Kim et al., 2016). However, few in vivo studies are conducted to investigate their antibiofilm activities.…”

“…pyogenes adhesion (Subramenium, Vijayakumar, & Pandian, 2015). Clove oil and eugenol inhibit more than 75% of biofilm formation in E. coli O157:H7, accompanied by the downregulated expression of type I fimbriae genes ( fimCDH ) and curli genes ( csgABDFG ), which are important for bacterial attachment (Kim et al., 2016). In addition, 50 µg/mL of allicin reduces the expression of fimH type I fimbriae gene of uropathogenic E. coli (UPEC) CFT073 and J96 by 64% and 77%, respectively, possibly due to the hydrogen bonds formed between allicin and two amino acids (Phe1 and Asn135) in FimH (Yang et al., 2016).…”

Progress on the Antimicrobial Activity Research of Clove Oil and Eugenol in the Food Antisepsis Field

“…Transcriptional analysis indicates that eugenol downregulates type I fimbriae genes (fimCDH), curli genes (csgABDFG), and ler‐controlled toxin genes (espD, escR, escJ, and tir), which play key roles on the biofilm formation, attachment, and effacement phenotype of the bacteria. However, clove oil and eugenol do not inhibit the biofilm formation of three laboratory E. coli K‐12 strains that reduced curli fimbriae production (Kim et al., ).…”

Escherichia coli, cattle and the propagation of disease

“…The first time when E. coli O157:H7 was linked to human outbreaks was in 1982, when two outbreaks of gastrointestinal illness caused by undercooked meat were reported and, prior to that, the same serotype was isolated in 1975 from a California woman who presented a self-limited gastrointestinal illness (Riley et al 1983). Since then, the bacterium became distributed globally, causing outbreaks, most of them community-acquired and transmitted by the foodborne and waterborne routes (Riley 2014;Munns et al 2015;Kim et al 2016). Escherichia coli O157 and E. coli O157:H7 may be acquired by person-to-person transmission (Spika et al 1986), the foodborne and waterborne routes, through farm visits and animal contact (Rangel et al 2005;Money et al 2010), from improperly chlorinated swimming pools (Friedman et al 1999) and from exposure while visiting petting zoos (Goode et al 2009).…”