Scripps research team blocks bacterial communication system to prevent deadly staph ...(f the Worm Institute for Research and Me...)

The genes turned on by quorum sensing may encode proteins harmless to their hosts, but they can also code for the toxins and other products arising from bacterial infections that cause disease. Sequestering autoinducers in some way could therefore block quorum sensing and, hence, the establishment of infections. The scientists predict that such a strategy would not lead to resistance in bacteria because it wouldn't kill the cells. Bacteria would simply remain in an inert form because they would be tricked into thinking not enough other cells were present to shift into their virulent mode.

Bacteria use a variety of genetic mechanisms in quorum sensing. The Scripps Research team focused on Gram-positive bacteria, whose quorum sensing is controlled by four basic types of autoinducers tied to a circuit known as the accessory gene regulator. Based on the known structure of one of these autoinducers, the team designed a molecule known as a hapten that, when conjugated with specific proteins using well-established procedures, induces the production of antibodies by the immune system.

The Janda group intentionally designed the hapten to be stable enough to work well as a potential treatment, and ultimately chose to pursue work with one of the haptens that proved the most stable. Past research by other groups has involved successfully blocking quorum sensing using molecules that essentially plug the keyholes on cell surfaces that allow bacteria to sense autoinducers, but such strategies have been hampered by the inherent instabilities of the molecules involved.

Next, the team isolated and studied the antibodies produced in mice injected with the hapten, called AP4. Subsequent experiments revealed that one of these antibodies in particular, when
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