Stopping MRSA before it becomes dangerous is possible, Sandia/UNM researchers find.
Most scientists believe that staph infections are caused by many bacterial cells that signal each other to emit toxins. The signaling process is called quorum sensing because many bacteria must be present to start the process. But the Jeff Brinker research group has determined that the very first stage of staph infection, when bacteria switch from a harmless to a virulent form, occurs in a single cell and that this individual process can be stopped by the application of a simple protein. The Brinker group's nonantibiotic approach may make it easier to treat staphylococci strains that have become drug resistant like the methicillin-resistant Staphylococcus aureus MRSA. The control of such strains is a formidable problem in hospitals. "The good news is that by inhibiting the single cell's signaling molecules with a small protein, we were able to suppress any genetic reprogramming into the bacterium's more virulent form," said Brinker. "Our work clearly showed the strategy worked." Brinker, with appointments at Sandia National Laboratories and the University of New Mexico, wrote about his group's findings in the Nov. 22 issue of Nature Chemical Biology. In the course of its experiments, the Brinker team achieved three firsts: They isolated Staphylococcus aureus bacteria in individual, self-assembled nanoscale compartments. Isolation of an individual bacterium previously had been achieved only computationally, leaving open questions of how a physically and chemically isolated bacterium would actually behave. They demonstrated that it was the release of signaling peptides from a single cell — not a quorum — that acted as a trigger to reprogram that same cell so that it released toxins. By introducing an inexpensive, very low-density lipoprotein (VLDL) to bind to the messenger peptide, they stopped the single cell from reprogramming itself.
