New Antibiotics Aim to Block Quorum Sensing

When these auto-inducers reach a certain threshold concentration, they interact with bacterial transcriptional regulators, thereby regulating gene expression.

Investigators at the University of Texas Southwestern Medical Center (Dallas, USA) had previously shown that the AI-3 quorum-sensing system is the mechanism by which E coli O157:H7 interacts with the eukaryotic hormones epinephrine/norepinephrine. This interaction activates the transcription of virulence genes in the bacteria.

In the current study, the investigators worked with a rabbit model to evaluate the ability of alpha and beta-adrenergic antagonists to interfere with the bacterial quorum sensing system. They reported in the June 27, 2006, online edition of the Proceedings of the [U.S.] National Academy of Sciences that the competitive nonselective alpha-adrenergic receptor antagonist. phentolamine bound to the E coli QseC receptor and prevented it from sensing the environmental signals that normally would have caused it to express its virulence genes.

"This receptor is found in many pathogens, so we can use this knowledge to design specific antagonists to block bacterial infections,” said senior author Dr. Vanessa Sperandio, assistant professor of microbiology at the University of Texas Southwestern Medical Center. "Overuse of antibiotics has led bacteria to develop resistance to antibiotics, so a novel type of therapy is needed.”



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