Phloretin Inhibits Quorum Sensing and Biofilm Formation in Serratia marcescens .
Yueheng QiPengcheng JiKunyuan YinYi ZhengJiangxiu NiuAiqun JiaJinwei ZhouHuayang FengPublished in: Molecules (Basel, Switzerland) (2023)
This study investigated the antivirulence capacity and mechanism of apple-skin-derived phloretin against Serratia marcescens NJ01, a vegetable spoilage bacterium. At 0.5 to 2 mg/mL doses, phloretin considerably inhibited the secretion of acyl homoserine lactones (AHLs), indicating that phloretin disrupted quorum sensing (QS) in S. marcescens NJ01. The dysfunction of QS resulted in reduced biofilms and the decreased production of protease, prodigiosin, extracellular polysaccharides (EPSs), and swimming and swarming motilities. Dysfunctional QS also weakened the activity of antioxidant enzymes and improved oxidative injury. The improved oxidative injury changed the composition of the membrane, improved membrane permeability, and eventually increased the susceptibility of biofilm cells to amikacin, netilmicin, and imipenem. The disrupted QS and enhanced oxidative stress also caused disorders of amino acid metabolism, energy metabolism, and nucleic acid metabolism, and ultimately attenuated the ability of S. marcescens NJ01 to induce spoilage. Our results indicated that phloretin can act as a potent drug to defend against spoilage by S. marcescens .
Keyphrases
- biofilm formation
- oxidative stress
- candida albicans
- pseudomonas aeruginosa
- induced apoptosis
- nucleic acid
- staphylococcus aureus
- amino acid
- escherichia coli
- anti inflammatory
- dna damage
- cystic fibrosis
- resting state
- endothelial cells
- wound healing
- emergency department
- signaling pathway
- cell death
- functional connectivity
- high resolution
- heat shock protein