Vitexin altersStaphylococcus aureussurface hydrophobicity to interfere with biofilm formation

Abstract

AbstractBacterial surface hydrophobicity is one of the determinant biophysical parameters of bacterial aggregation for being networked to form biofilm. Phytoconstituents like vitexin have long been in use for their antibacterial effect. The present work is aimed to characterise the effect of vitexin onS. aureussurface hydrophobicity and corresponding aggregation to form biofilm. We have found that vitexin shows minimum inhibitory concentration at 252 μg/ml againstS. aureus.Vitexin reduces cell surface hydrophobicity and membrane permeability at sub-MIC dose of 126 μg/ml. Thein silicobinding analysis showed higher binding affinity of vitexin with surface proteins ofS. aureus.Down regulation ofdltA,icaAB and reduction in membrane potential under sub-MIC dose of vitexin, explains reducedS. aureussurface hydrophobicity. Vitexin has substantially reduced the intracellular adhesion of planktonic cells to form biofilm through interference of EPS formation, motility and subsequent execution of virulence. This was supported by the observation that vitexin down regulates the expression oficaAB andagrAC genes ofS. aureus.In addition, vitexin also found to potentiate antibiofilm activity of sub-MIC dose of gentamicin and azithromycin. Furthermore, CFU count, histological examination of mouse tissue and immunomodulatory study justifies thein vivoprotective effect of vitexin fromS. aureusbiofilm associated infection. Finally it can be inferred that, vitexin has the ability to modulateS. aureuscell surface hydrophobicity which can further interfere biofilm formation of the bacteria.ImportanceThere has been substantial information known about role of bacterial surface hydrophobicity during attachment of single planktonic bacterial cells to any surface and the subsequent development of mature biofilm. This study presents the effect of flavone phytoconstituent vitexin on modulation of cell surface hydrophobicity in reducing formation of biofilm. Our findings also highlight the ability of vitexin in reducingin vivo S. aureusbiofilm which will eventually outcompete the correspondingin vitroantibiofilm effect. Synergistic effect of vitexin on azithromycin and gentamicin point to a regime where development of drug tolerance may be addressed. Our findings explore one probable way of overcoming drug tolerance through application of vitexin in addressing the issue ofS. aureusbiofilm through modulation of cell surface hydrophobicity.