Impact of quorum sensing signaling molecule AI-2 and quorum sensing inhibitors on Escherichia coli drug resistance and their application in spoilage of chilled pork

Abstract

Quorum sensing (QS) is closely related to bacterial drug resistance. The relationship between the evolution of drug resistance and QS of Escherichia coli needs to be deeply analyzed. From the perspective of QS, this study aimed to explore the effects of quorum sensing signal molecule (QSSM) autoinducer-2 (AI-2) and quorum sensing inhibitors (QSIs, cinnamaldehyde and eugenol) on drug resistance of E. coli, and their application on chilled pork. Upon exposure to 1 μM AI-2, the drug-resistance related genes (TEM, ompF, acrB) were differentially expressed, and the E. coli strains were changed from sensitivity to resistance on ampicillin, leading to the faster growth compared to control strains under 1/2 minimum inhibitory concentration (MIC). On the other hand, cinnamaldehyde and eugenol (1/2MIC) could inhibit at least 40 % of AI-2 activity. They could reverse regulate the expression of resistance genes compared to AI-2, restrain the biofilm formation, and cause intracellular materials leakage. These results provide evidence that cinnamaldehyde and eugenol may negatively regulate QS by inhibiting AI-2 activity, thereby affecting the drug resistance of E. coli. In food samples, the chilled pork inoculated with drug-resistant E. coli was treated with AI-2, cinnamaldehyde or eugenol. It was determined that QSIs delay the growth of microorganisms, slow down the increase in pH and TBARS values, reduce the rate of water loss, and protect color. On the contrary, the AI-2 treatment group was not conducive to the preservation of chilled pork. These findings provide new insights into the relationship of QS and drug-resistance of E. coli.