Quorum sensing (QS) is the well adapted cell to cell communication system present mainly in all the pathogenic bacterial species. The mechanism of QS is population-density-dependent and the system expresses at particular threshold signal. This system regulates the production of N-acylated l-homoserine lactones (AHLs) as autoinducers (AIs) which mediate the QS signalling pathway. QS activity is responsible for the production of virulence factors, formation of bacterial biofilm and directly associated with the development of drug resistance. Phenolic compounds from the ginger rhizome (Zingiber officinale Roscoe) viz. [6]-gingerol, [6]-shogaol and isoxazoline derivative of [6]-gingerol exhibited QS inhibitory activity against Chromobacterium violaceum and Pseudomonas aeruginosa and thus found to be the promising leads in the domain of anti pathogenic drugs. In this work we have focussed our attention on the identification of mode of binding of phenolic compounds (those showing anti QS activity) of ginger rhizome in the active site pockets of CviR and LasR receptor protein. Based on this template, molecular docking of analysis of polyphenolic compounds (stilbenes, flavonols, flavan-3-ols) which are abundantly present in Vitis vinifera (common grape vine) was carried out. Out of 9 studied bioactives majorly all of them were found to be effectively stabilizing the domain of LasR receptor protein and binding with greater affinity (-6.8 to -11.4 kcal/mol) in comparison to natural ligand. The best binding affinity was shown by quercetin and myricetin which belongs to flavonols. However, in general polyphenolic compounds have shown less binding affinity against CviR receptor protein. Further, molecular electrostatic surface potential (MESP) of the investigated compounds have shown that polyphenols carry structural complementary features which are responsible for the binding interaction with the target proteins. Present study illustrated the potential of polyphenolic compounds present in Vitis vinifera to act as prospective leads for the further development of novel QS inhibitors as antimicrobial therapeutics.