Abstract
Serratia marcescens is one of the important nosocomial pathogens which rely on quorum sensing (QS) to regulate the production of biofilm and several virulence factors. Hence, blocking of QS has become a promising approach to quench the virulence of S. marcescens. For the first time, QS inhibitory (QSI) and antibiofilm potential of Actinidia deliciosa have been explored against S. marcescens clinical isolate (CI). A. deliciosa pulp extract significantly inhibited the virulence and biofilm production without any deleterious effect on the growth. Vanillic acid was identified as an active lead responsible for the QSI activity. Addition of vanillic acid to the growth medium significantly affected the QS regulated production of biofilm and virulence factors in a concentration dependent mode in S. marcescens CI, ATCC 14756 and MG1. Furthermore vanillic acid increased the survival of Caenorhabditis elegans upon S. marcescens infection. Proteomic analysis and mass spectrometric identification of differentially expressed proteins revealed the ability of vanillic acid to modulate the expression of proteins involved in S-layers, histidine, flagellin and fatty acid production. QSI potential of the vanillic acid observed in the current study paves the way for exploring it as a potential therapeutic candidate to treat S. marcescens infections.
Highlights
Light and CLSM microscopic analyses further confirmed the antibiofilm activity of vanillic acid against S. marcescens CI, S. marcescens ATCC and S. marcescens MG1 used in this study
FTIR analysis of EPS extracted from control and vanillic acid treated S. marcescens CI showed the reduction in the nucleic acid, amide I and II proteins and fatty acid content
In vivo assays confirms the ability of vanillic acid to rescue C. elegans form the S. marcescens CI, S. marcescens ATCC and S. marcescens MG1 infection by inhibiting the QS regulated virulence and biofilm formation
Summary
In the present study, we have evaluated the effect of vanillic acid treatment on the osmotic stress resistance of S. marcescens and the results revealed that vanillic acid treated cells are unable to grow normally in the presence of 0.5 and 1 M NaCl when compared to control. These results suggest the ability of vanillic acid to modulate the osmotic stress resistance in S. marcescens by down regulating the expression of slaA protein.
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