Abstract
The presence of Staphylococcus epidermidis biofilms on medical devices is a major cause of nosocomial diseases and infections. Extensive research is directed at inhibiting the formation and maturation of such biofilms. Natural plant-derived phenolic compounds have promising antimicrobial effects against drug-resistant bacteria. The anti-biofilm activity of two selected phenolic compounds (vanillin and syringic acid) was tested against three biofilm-forming methicillin-resistant S. epidermidis strains with different genotypes. Resazurin assay combining crystal violet staining and confocal microscopy was used for biofilm and extracellular polymer substance (EPS) inhibition tests. Effects on EPS compounds such as proteins, extracellular DNA, and polysaccharides were also examined. Combined with quantitative real-time PCR of selected agr quorum-sensing systems and biofilm genetic determinants, our complex analysis of vanillin and syringic acid showed similar biofilm and EPS inhibition effects on S. epidermidis strains, reducing biofilm formation up to 80% and EPS up to 55%, depending on the genotype of the tested strain. Natural antimicrobial agents are thus potentially useful inhibitors of biofilms.
Highlights
IntroductionIn contrast to Staphylococcus aureus, which expresses a broad spectrum of virulence factors, the main strategy of S. epidermidis is biofilm formation leading to the spread of chronic or acute infections [1,2]
Staphylococcus epidermidis is an opportunistic pathogen of human microflora
Since the minimal inhibition concentrations (MICs) for all four analyzed phenolic compounds were determined at different concentrations, subinhibitory concentrations are indicated in this work as 1/60, 1/40, and 1/20 MIC
Summary
In contrast to Staphylococcus aureus, which expresses a broad spectrum of virulence factors, the main strategy of S. epidermidis is biofilm formation leading to the spread of chronic or acute infections [1,2]. QS as a cellular communication system used by bacterial pathogens coordinates biofilm formation and the production of virulence factors [8,9]. In S. epidermidis, the agr (accessory gene regulator) system is considered a prototype of the QS mechanism. The P3 promoter controls the production of the 510-nucleotide-long RNAIII intracellular effector molecule of the agr QS system [13] and is responsible for the regulation of the system itself [14] and of many virulence factors and biofilm proteases such as EcpA, EspA, and
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