"Right now, we have very little idea of the mechanism at work here. Perhaps as an enzyme Rv3671c cleaves a transcription regulator that then turns on some kind of defensive program within the bacterium. Only further study will reveal those secrets," says Dr. Ehrt.
"What is clear is that by targeting an element involved directly in the infective process, we may develop a line of drugs that work in collaboration with, rather than in difference to, the host environment, including host immune responses," Dr. Nathan says. "Hopefully, this kind of approach can help solve the ongoing problem of bacterial drug resistance."
The new study is also another example of an interdisciplinary approach -- this time among biochemists, microbiologists, immunologists and cell biologists.
"In the ideal collaboration, each participant brings key insights from their particular discipline to the table," Dr. Nathan says. "The results are discoveries like these."
|Contact: Andrew Klein|
New York- Presbyterian Hospital/Weill Cornell Medical Center/Weill Cornell Medical College