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Anti-virulent Disruption of Pathogenic Biofilms using Engineered Quorum-quenching Lactonases
Published on: January 1, 2016
Phloretin Inhibits Quorum Sensing and Biofilm Formation in Serratia marcescens
Yueheng Qi1,2, Pengcheng Ji3, Kunyuan Yin3
1Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou 477150, China.
Abstract:
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.
Insights
Apple-derived phloretin disrupts quorum sensing (QS) in Serratia marcescens, reducing spoilage. This antivirulence strategy weakens bacterial defenses and increases antibiotic susceptibility.
Area of Science:
- Microbiology
- Food Science
- Biochemistry
Background:
- Serratia marcescens is a bacterium that causes vegetable spoilage.
- Quorum sensing (QS) is a cell-to-cell communication system bacteria use to coordinate virulence.
- Phloretin is a natural compound found in apple skins.
Purpose of the Study:
- To investigate the antivirulence effects of phloretin against S. marcescens.
- To elucidate the mechanism by which phloretin inhibits S. marcescens.
Main Methods:
- Bacterial cultures of S. marcescens NJ01 were treated with phloretin at varying concentrations.
- Acyl homoserine lactone (AHL) secretion was measured to assess QS inhibition.
- Biofilm formation, protease production, prodigiosin, motility, and oxidative stress were evaluated.
- Membrane permeability and susceptibility to antibiotics were assessed.
- Metabolic pathways (amino acid, energy, nucleic acid) were analyzed.
Main Results:
- Phloretin (0.5-2 mg/mL) inhibited AHL secretion, disrupting QS in S. marcescens.
- QS disruption led to reduced biofilms, protease, prodigiosin, and motility.
- Antioxidant enzyme activity decreased, increasing oxidative injury and membrane damage.
- Enhanced oxidative stress increased susceptibility to amikacin, netilmicin, and imipenem.
- Disrupted QS and oxidative stress disordered key metabolic pathways, reducing spoilage ability.
Conclusions:
- Phloretin effectively inhibits S. marcescens virulence by disrupting QS.
- Phloretin's mechanism involves increased oxidative stress and metabolic disruption.
- Phloretin shows potential as a natural agent to prevent S. marcescens-induced spoilage.
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