You've probably heard that all the antibiotics we take are breeding new generations of drug-resistant bacteria. In fact, many diseases we once killed easily with Penicillin now require mega-doses of super-antibiotics like Cipro. While researchers have known for a long time that bacteria are developing resistance to drugs, they weren't sure how the tiny organisms did it. Now a research team at the University of Illinois has figured it out — and that means we're like to see new, smarter antibiotics (you can see the chemical structure of one such antibiotic, Erythromycin, at left).
A release from the University of Illinois explains:
Erythromycin and newer macrolide antibiotics azithromycin and clarithromycin are often used to treat respiratory tract infections, as well as outbreaks of syphilis, acne and gonorrhea. The drugs can be used by patients allergic to penicillin.This is good news for many of us who have been worried about antibiotic resistance. It could mean a more targeted method of killing dangerous bacteria in our bodies, and a future without mega-infections.
Macrolide antibiotics act upon the ribosomes, the protein-synthesizing factories of the cell. A newly-made protein exits the ribosome through a tunnel that spans the ribosome body. Antibiotics can ward off an infection by attaching to the ribosome and preventing proteins the bacterium needs from moving through the tunnel.
Some bacteria have learned how to sense the presence of the antibiotic in the ribosomal tunnel, and in response, switch on genes that make them resistant to the drug, Mankin said. The phenomenon of inducible antibiotic expression was known decades ago, but the molecular mechanism was unknown.
Mankin and his team of researchers — Nora Vazquez-Laslop, assistant professor in the Center for Pharmaceutical Biotechnology, and undergraduate student Celine Thum — used new biochemical and genetic techniques to work out the details of its operation.
"Combining biochemical data with the knowledge of the structure of the ribosome tunnel, we were able to identify some of the key molecular players involved in the induction mechanism," said Vazquez-Laslop.
"We only researched response to erythromycin-like drugs because the majority of the genetics were already known," she said. "There may be other antibiotics and resistance genes in pathogenic bacteria regulated by this same mechanism. This is just the beginning."
UIC scientists discover why some bacteria resist antibiotics [Eurekalert]