Biofilm genesis by Pseudomonas and Staphylococcus sp is associated with biofouling in natural settings. D-Tryptophan (D-Trp) inhibits bacterial biofilms and have been proposed for biofouling control applications. In this study,… Click to show full abstract
Biofilm genesis by Pseudomonas and Staphylococcus sp is associated with biofouling in natural settings. D-Tryptophan (D-Trp) inhibits bacterial biofilms and have been proposed for biofouling control applications. In this study, D-Trp significantly inhibited Pseudomonas mendocina and Staphylococcus aureus cell attachment (biofilm formation) rates on polystyrene 96-well microtiter plates in comparison with L-Tryptophan (L-Trp) and mixtures of D-/L-Tryptophan (D-/L-Trp). The inhibitory effect was greater on P. mendocina, where the rate of cell adherence was declined to 8.7 × 105 cells/h from 8.0 × 106 cells/h (control) in P. mendocina. In S. aureus it was declined to 4.2 × 107 cells/h from 9.2 × 107 cells/h (control) at 1 mM concentration. It hindered the intracellular communication and adherence in both the strains, as confirmed by SEM and real time PCR analysis. Addition of D-Trp to preformed biofilms also caused partial disassembly. Intra and interbacterial aggregation were decreased subsequently upon treatment with D-Trp. It repressed the genes involved in cell–cell communication, which could be responsible for the diminished biofilm formation of the selected strains. Hence D-Tryptophan has proved to be an effective strategy to control biofilm and may support in the development of surface coating technologies.
               
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