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"Figuring out how to synthesize these signal molecules so that we could do the dispersal experiments was a real breakthrough," he said. "We used this new method to make AIP, added it directly to established biofilms and watched them blow apart. And that's when the excitement started."

Having established that activation of the quorum-sensing system in established biofilms triggers dispersal of the biofilm, the UI team has started to investigate the details of the mechanism. In particular, they discovered the mechanism depended on the presence of active proteases -- enzymes that break down proteins.

"If we can learn more about how the system works, then that might suggest new therapeutic targets," said Blaise Boles, Ph.D., UI postdoctoral research fellow.

Importantly, Horswill and Boles also showed that bacteria released from the biofilm were once again susceptible to antibiotics, which raises possibilities for improving treatments for chronic biofilm infections.

"Current treatment for endocarditis -- a potentially life threatening infection where a staph biofilm forms on heart valves -- involves weeks of intravenous antibiotics, and sometimes requires surgery," Boles explained. "One thing we'd like to test is whether we can treat biofilms in models of diseases like endocarditis by turning on quorum sensing."

Horswill added that he plans to start a collaborative effort with Jose Morcuende, M.D., Ph.D., UI associate professor of orthopaedics and rehabilitation, to investigate the dispersal of staph biofilms from both allograft bone and medical implant materials.

The findings also may have implications for treating biofilms of emerging antibiotic resistant staph strains, including methicillin-resistant Staphylococcus aureus (MRSA).

Although the team has not tested their dispersal methods on MSRA, Horswill note
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