University of Iowa researchers have succeeded in wiping out established biofilms of Staphylococcus aureus (staph) by hijacking one of the bacteria's own regulatory systems. Although the discovery is not ready for clinical application, the findings offer insight into a dispersal mechanism for staph biofilms and might help identify therapeutic targets.
Biofilms are communities of bacteria that grow on moist surfaces, including heart valves, bone and medical implants. Encased in self-produced slime and highly resistant to antibiotic therapy and the body's own immune defenses, biofilm infections represent a tough and dangerous medical problem. The findings were published in the journal Public Library of Science Pathogens (PLoS-Pathogens) on April 25.
"We have shown that activating the cells' communication system, also known as quorum sensing, in established biofilms causes the biofilms to disperse rapidly," said Alexander Horswill, Ph.D., UI assistant professor of microbiology and senior study author. "This is the first report of an existing dispersal pathway in Staph aureus. If we can tap into this mechanism, then that might lead to better treatments."
Quorum sensing is the mechanism bacteria use for cell-to-cell signaling. This communication system allows bacteria to react to environmental changes in order to survive and thrive. In Staphylococcus aureus, the quorum-sensing system is turned on by autoinducing peptides (AIPs), small molecules that contain an unusual cyclic structure and are shaped like a ring with a tail.
Previous research, including work done at the UI, suggested that this quorum-sensing system was involved in biofilm detachment, but it was difficult to test the idea because there was no good way to make AIPs.
That is where Horswill's expertise came in. In earlier research he had developed an enzymatic approach for manufacturing cyclic peptides. Using this chemistry, he was able to prepare large qua
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University of Iowa