Abstract
Interference with bacterial quorum sensing communication provides an anti-virulence strategy to control pathogenic bacteria. Here, using the Enteropathogenic E. coli (EPEC) O103:H2, we showed for the first time that thiophenone TF101 reduced expression of lsrB; the gene encoding the AI-2 receptor. Combined results of transcriptional and phenotypic analyses suggested that TF101 interfere with AI-2 signalling, possibly by competing with AI-2 for binding to LsrB. This is supported by in silico docking prediction of thiophenone TF101 in the LsrB pocket. Transcriptional analyses furthermore showed that thiophenone TF101 interfered with expression of the virulence genes eae and fimH. In addition, TF101 reduced AI-2 induced E. coli adhesion to colorectal adenocarcinoma cells. TF101, on the other hand, did not affect epinephrine or norepinephrine enhanced E. coli adhesion. Overall, our results showed that thiophenone TF101 interfered with virulence expression in E. coli O103:H2, suggestedly by interfering with AI-2 mediated quorum sensing. We thus conclude that thiophenone TF101 might represent a promising future anti-virulence agent in the fight against pathogenic E. coli.
Highlights
Bacteria communicate via signal molecules either produced by the bacteria themselves, by the host organism or molecules in the environment
We have previously shown that biofilm formation and motility in E. coli O103:H2 are reduced by both furanone F202 [35, 36], and its sulfur analogue thiophenone TF101 [35], with TF101 being the most efficacious [35]
The possible interference of thiophenone with the AI-2 signaling system was investigated by measuring expression of the lsrB gene, encoding the AI-2 binding receptor, using quantitative real-time PCR with samples collected after 2 hours of exposure to AI-2, TF101 or AI-2 and TF101 in combination
Summary
Bacteria communicate via signal molecules either produced by the bacteria themselves, by the host organism or molecules in the environment. One such process of bacterial cell-cell signaling is quorum sensing (QS), that enables bacteria to sense and respond according to cell population density, and to regulate virulence gene expression [1, 2]. The autoinducer-2 (AI2) QS molecule is one of the most extensively studied, and AI-2 has been recognized as an intra- and inter-species communication signal. The substrate of LuxS is S-Ribosylhomocysteine, which is cleaved to yield homocysteine and 4, 5-dihydroxy-2, 3- pentandione (DPD). DPD cyclizes spontaneously to form AI-2 [7]
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