, 2002; Gonzalez Barrios et al., 2006). Escherichia coli O157:H7 harbors QS-regulated virulence genes on a pathogenicity island termed the locus of enterocyte effacement (LEE) (Surette & Bassler, 1998) that is organized mainly into the five polycistronic operons LEE1–LEE5 (Kaper et al., 2004). The first gene in LEE1, LEE-encoded regulator (ler), produces the principal transcriptional activator of the LEE genes (Elliott et al., 2000) and its expression was reported to be positively regulated by both AI-3 and norepinephrine (Sperandio et al., 2003; Jelcic et al., 2008). In patients with E. coli O157:H7 infection,

antibiotic use is generally limited because bacterial cells lysed by antibiotic treatment release MS275 an excessive quantity of Shiga toxin, thereby aggravating the patient’s state and resulting in HUS (Wong et al., 2000). To avoid this risk, an antimicrobial treatment that involves attenuation of bacterial virulence by inhibiting QS has been proposed (Ren et al., 2004). Halogenated furanone compounds as QS inhibitors were isolated from marine macroalga, Delisea pulchra (Givskov et al., 1996). Many of the synthesized furanone

derivatives have also been identified as QS inhibitors both in vitro (Martinelli et al., 2004) and in vivo (Wu et al., 2004). However, most of the characterized QS inhibitors have not yet been qualified as chemotherapeutic agents because they are composed see more of halogens that exert toxic effects in humans. Thus, more efforts should be made to develop safer QS inhibitors from natural products. As a soluble fiber, broccoli (Brassica oleracea) contains a large amount of vitamin C and multiple mafosfamide nutrients with potent anticancer properties (Vasanthi et al., 2009). However, the effect of broccoli against infection by pathogenic bacteria has never been reported. In this study, we demonstrate the inhibitory effects of broccoli extract (BE) on bacterial QS using E. coli O157:H7 as a model organism. The in vivo effects of the BE against E. coli O157:H7 infection were also elucidated in a Caenorhabditis elegans killing

assay. Finally, we tested three different flavonoid compounds (quercetin, kaempferol and myricetin) reported to be present in BE (He et al., 2008; Schmidt et al., 2010) in order to gain better insight into the active inhibitory compound in BE. An E. coli O157:H7 strain ATCC 43894 producing Shiga toxins I and II, an avirulent E. coli OP50 strain and Chromobacterium violaceum CV026 were grown in Luria–Bertani broth (LB, 10 g tryptone, 5 g NaCl, 5 g yeast extract L−1) at 37 °C. Vibrio harveyi BB170, an AI-2 reporter strain, was grown at 30 °C with agitation (175 r.p.m.) in the AB medium (Fong et al., 2001). The AB medium consisted of 10 mM potassium phosphate (pH 7.0), 0.3 M NaCl, 0.05 M MgSO4, 0.2% Casamino acids (Difco), 2% glycerol, 1 mM l-arginine, 1 μg mL−1 of thiamine, and 0.01 μg mL−1 of riboflavin. Quercetin, kaempferol and myricetin were purchased from Sigma-Aldridge (St.