We assessed the quorum sensing (QS) inhibitory impact of sesamol against the foodborne bacterium Pseudomonas aeruginosa. At concentrations ranging from 50 to 200 μg/mL, sesamol significantly inhibited the production of virulence factors such as protease, elastase, pyocyanin, rhamnolipid, and chemotaxis, and improved the susceptibility of bacterial and biofilm cells to colistin. Integrated transcriptomics, metabolomics, and docking analyses indicated that exposure to sesamol destroyed the QS system and down-regulated the expressions of genes encoding virulence and antioxidant enzymes. The down-regulation of genes encoding antioxidant enzymes intensified oxidative stress, as demonstrated by the enhancement of reactive oxygen species and H₂O₂. The enhanced oxidative stress changed the components of the cell membrane, improved its permeability, and ultimately enhanced the susceptibility of bacterial and biofilm cells to colistin. Moreover, exposure to sesamol also led to the disorder of amino acid metabolism and energy metabolism, eventually attenuating the pathogenicity of P. aeruginosa. These findings indicated that sesamol can function as a potent anti-virulence agent to defend against food spoilage caused by P. aeruginosa.

Pseudomonas aeruginosa is a significant contributor to food spoilage and foodborne diseases. The primary strategy for preventing and controlling contamination by P. aeruginosa involves the application of antibacterial agents. However, the overuse or abuse of antimicrobial agents has accelerated the development of drug resistance. The control of spoilage and antimicrobial resistance in P. aeruginosa has emerged as a major food safety challenge. Numerous studies have established that the pathogenicity and drug resistance of P. aeruginosa are regulated by quorum sensing (QS). Therefore, inhibiting the QS system of P. aeruginosa is a promising approach to mitigate the pathogenicity and resistance of this pathogen. This review explores various QS systems of P. aeruginosa and their roles in bacterial pathogenesis and drug resistance. Additionally, it discusses the potential of small chemical molecules and quorum-quenching enzymes in attenuating the pathogenesis of P. aeruginosa, as well as the possibility of using QS inhibitors (QSIs) and antibiotics in future therapeutic approaches for P. aeruginosa-associated infections.

Serratia marcescens is a common opportunistic pathogen that causes infections in clinical patients. The aim of this study was to investigate the inhibitory efficiency of carvone on the production of virulence factors and evaluated the susceptibility of antibiotics against biofilms of S. marcescens in combination with carvone. Carvone treatment notably inhibited the production of lipase, prodigiosin, extracellular polysaccharides (EPS), and swimming and swarming motilities. Carvone exposure also reduced the formation of biofilms in S. marcescens NJ01. When exposed to antibiotics in combination with carvone, the inhibitory impact was notably improved. In addition, the expressions of genes glp and katG involved in the synthesis of glutathione peroxidase and catalase, respectively, were significantly suppressed after treatment with carvone. The suppression of antioxidant enzymes resulted in the improvement of reactive oxygen species (ROS) and H₂O₂, enhanced the permeability of membrane, and eventually increased the susceptibility of biofilms or planktonic cells to antibiotics. The data mentioned above indicated that carvone is expected to play an important role in the control and treatment of S. marcescns infection.