Bacteria communicate within a system by means of a density dependent mechanism known as quorum sensing which regulate the metabolic and behavioral activities of a bacterial community. This sort of interaction occurs through a dialect of chemical signals called as autoinducers synthesized by bacteria. Bacterial quorum sensing occurs through various complex pathways depending upon specious diversity. Therefore the cognizance of quorum sensing mechanism will enable the regulation and thereby constrain bacterial communication. Inhibition strategies of quorum sensing are collectively called as quorum quenching; through which bacteria are incapacitated of its interaction with each other. Many virulence mechanism such as sporulation, biofilm formation, toxin production can be blocked by quorum quenching. Usually quorum quenching mechanisms can be broadly classified into enzymatic methods and non-enzymatic methods. Substantial understanding of bacterial communication and its inhibition enhances the development of novel antibacterial therapeutic drugs. In this review we have discussed the types and mechanisms of quorum sensing and various methods to inhibit and regulate density dependent bacterial communication.

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Bacterial virulence is controlled by a cascade of genes influenced by quorum sensing alias bacterial signalling.The present study was intended to develop an effective module that could constrain bacterial communication without harming the host. Quorum quenching ability of Tribulus terrestris was screened upon chromogenic reporter strains such as Chromobacterium violaceum, Serratia marcescens and Pseudomonas aeruginosa. Hydro-alcoholic extracts of root showed positive quorum quenching activity by effectively down regulating quorum sensing controlled mechanisms such as pigment production and biofilm formation. Lead component was purified and found to be ß-1, 5-O-dibenzoyl ribofuranose by GC-MS NIST and NMR spectrometry. Interestingly it was observed that the compound was neither bactericidal nor bacteriostatic but rather it's only disturbing its interaction. Further studies revealed that the antagonist is not inhibiting the production of signalling molecule acyl homoserine lactone, instead inhibiting its action.

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