Turning on cell-cell communication wipes out staph biofilms

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 notes that the MRSA stains are quite similar to the lab strains he and Boles tested and have quorum-sensing systems that are even more active than those of the lab strains. This suggests that MRSA might be particularly sensitive to approaches that manipulate quorum sensing.

Moving a basic discovery into medically relevant experimental models is an example of translational research of the type supported and encouraged by the new Institute for Clinical and Translational Science at the UI.

The study was funded in part by the Cystic Fibrosis Foundation and the Roy J. Carver Charitable Trust of Muscatine, Iowa.

STORY SOURCE: University of Iowa Health Science Relations, 5135 Westlawn, Iowa City, Iowa 52242-1178

MEDIA CONTACTS: Alexander Horswill, microbiology, ; Jennifer Brown, UI Health Care Media Relations, 319-335-9917,