Science & tech · 2007

Can a chemical disrupt bacterial communication and reduce harmful products without slowing bacterial growth?

Yes—in laboratory tests with Pseudomonas aeruginosa PAO1, C10-CPA inhibited quorum sensing, production of several virulence factors, and biofilm formation without affecting bacterial growth. It was the strongest quorum-sensing inhibitor among the C8-CPA analogs tested.

Details

N-octanoyl cyclopentylamide (C8-CPA) was found to moderately inhibit quorum sensing, a form of bacterial communication, in Pseudomonas aeruginosa PAO1. To obtain stronger inhibitors, researchers conducted a laboratory experiment: they synthesized a series of structural analogs of C8-CPA and tested their ability to inhibit quorum sensing in P. aeruginosa PAO1.

The lasB-lacZ and rhlA-lacZ reporter assays showed that chain length and ring structure were critical to the analogs’ ability to inhibit quorum sensing. N-decanoyl cyclopentylamide (C10-CPA) was the strongest inhibitor tested. The concentrations required for half-maximal inhibition of lasB-lacZ and rhlA-lacZ expression were 80 and 90 µM, respectively.

C10-CPA also inhibited production of the virulence factors elastase, pyocyanin, and rhamnolipid, as well as biofilm formation, without affecting the growth of P. aeruginosa PAO1.

In a lasI rhlI mutant of P. aeruginosa PAO1, C10-CPA inhibited both the induction of lasI-lacZ by N-(3-oxododecanoyl)-L-homoserine lactone (PAI1) and the induction of rhlA-lacZ by N-butanoyl-L-homoserine lactone (PAI2). These findings indicate that C10-CPA interferes with the las and rhl quorum-sensing systems by inhibiting interactions between their response regulators, LasR and RhlR, and autoinducers.

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