Lactobacillus acidophilus reduces expression of enterohemorrhagic Escherichia coli O157:H7 virulence factors by inhibiting autoinducer-2-like activity

Recent investigations have shown that many pathogenic bacteria have quorum sensing (QS) systems to coordinate virulence factors, pointing out a new, promising target for anti-microbial drugs. In the present study, by interfering with autoinducer (AI)-2-like activity, we investigated the effects of cell extracts isolated from Lactobacillus on the virulence of enterohemorrhagic Escherichia coli (EHEC) O157:H7, including attachment, biofilm formation, and the killing of a surrogate host, the nematode Caenorhabditis elegans. In the AI-2 bioassay, profound inhibitions of AI-2-like activity were exerted on EHEC O157:H7 ATCC 43894 in the presence of the 1.0% (w/v) Lactobacillus acidophilus A4 cell extract, whereas the growth of EHEC was not changed. By adding the cell extract, inhibitory effects were exhibited on epithelial cell attachment, as well as on biofilm formation on abiotic surfaces, whereas significant reductions in EHEC O157:H7 pathogenicity were not observed in the C. elegans nematode in vivo model. In the comparative proteomic analysis, the 1.0% cell extract down-regulated expression of several virulence factors controlled by AI-2-like activity. In particular, these proteins have consistent roles in membrane associated functions and sulfur metabolism.