Propolis Stops Bacterial Growth Proven by Quorum Sensing

a very technical explanation confirming the fact that Propolis is effective at stopping bacterial growth; thus the reason for its reputation of being antibacterial... 

A Novel Property of Propolis (Bee Glue): Anti-Pathogenic Activity by Inhibition of N-acyl-Homoserine Lactone Mediated Signaling in Bacteria

Journal ofEthnopharmacology, In Press, Accepted

An alternative approach to antibiotics is the development of anti-pathogenic agents to control the bacterial virulome. Such anti-pathogenic agents could target a phenomena known as quorum sensing (QS).

Materials and Methods

Six bacterial N-acyl-homoserine lactone (AHL)-dependent bioreporter strains were used to evaluate if bee hive glue also known as propolis contains constituents that capable of inhibiting QS-controlled AHL signaling. In addition, the effect of propolis on the QS-dependent swarming motility was evaluated with the opportunisitic pathogen, Pseudomonas aeruginosa.

Results

Differences in the propolis tinctures samples were identified by physiochemical profiles and absorption spectra. Propolis tinctures at 0.0005% v/v that do not affect bacteria biosensor growth or the reporter system monitored were exposed to biosensors with and without the addition an AHL. No AHL signal mimics were found to be present in the propolis tinctures. However, when propolis and an inducer AHL signal were together exposed to five E.coli and a Chromobacterium violaceum biosensor, propolis disrupted the QS bacterial signaling system in liquid- and agar-based bioassays and in C18 reverse-phase thin-layer plate assays. Swarming motility in the opportunistic pathogen, P. aeruginosa PAO1 and its AHL-dependent LasR- and RhlR-based QS behaviors were also inhibited by propolis.

Conclusions

Together, we present evidence that propolis contain compounds that suppress QS responses. In this regard, anti-pathogenic compounds from bee harvested propolis could be identified and isolated and thus will be valuable for the further development of therapeutics to disrupt QS signaling systems which regulate the virulome in many pathogenic bacteria.