Boston University biomedical engineers find chink in bacter...( Biomedical researchers at Boston Uni...)

Biomedical researchers at Boston Universitys College of Engineering may have discovered the path toward developing better drugs capable of defeating so-called superbugs, bacteria that have developed resistance to common antibiotics. The researchers have discovered a previously unknown chain of events occurring in bacteria that opens to door to new avenues of research.

Currently, three classes of bactericidal antibiotics are used to target different bacterial functions: inhibiting DNA replication; blocking protein-building; or halting construction of cell walls. Research from the laboratory of Professor James Collins found the three classes more alike than anyone realized, and the commonalities may be the bugs downfall.

Collins and colleagues article, A Common Mechanism of Cellular Death Induced by Bactericidal Antibiotics, appears in the September 7 issue of Cell.

The researchers discovered a common process, or pathway, that was triggered by all three types of antibiotics. Theres an underlying pathway beyond the drug interacting with the target, said graduate student and lead author Michael Kohanski, and the endpoint of this pathway is excessive free radical production.

Free radicals -- such as hydroxyl or superoxide radicals -- are molecules that carry a free, or unpaired, electron like a weapon. Theyll damage DNA, proteins, lipids in the membrane, pretty much anything. Theyre equal opportunity damagers, said Kohanski.

This hidden pathway and resultant free radical overload appears to help current antibiotics do their job, but is not always enough to kill all bacteria by itself. Collins group theorizes that if this effect can be amplified, or if the cells genetic defense against it can be weakened, no bacteria could withstand its effect and the emergence of antibiotic-resistant bacteria could be limited.

Importantly, we showed that if you can inhibit or block the bacterial defense mechanisms to hydrox
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