Skip to comments.An antibiotic effect minus resistance
Posted on 10/28/2011 11:04:07 AM PDT by decimon
Researcher's compound disables bacteria instead of killing them
After 70 years, antibiotics are still the primary treatment for halting the spread of bacterial infections. But the prevalence of antibiotic resistance is now outpacing the rate of new drug discovery and approval.
A microbiologist at the University of Wisconsin-Milwaukee (UWM) has discovered a different approach: Instead of killing the bacteria, why not disarm them, quashing disease without the worry of antibiotic resistance?
Ching-Hong Yang, associate professor of biological sciences, has developed a compound that shuts off the "valve" in a pathogen's DNA that allows it to invade and infect.
The research is so promising that two private companies are testing it with an eye toward commercialization.
"We analyzed the genomic defense pathways in plants to identify all the precursors to infection," says Yang. "Then we used the information to discover a group of novel small molecules that interrupt one channel in the intricate pathway system."
Yang and collaborator Xin Chen, a professor of chemistry at Changzhou University in China, have tested the compound on two virulent bacteria that affect plants and one that attacks humans. They found it effective against all three and believe the compound can be applied to treatments for plants, animals and people.
The work was published online this month in the journal Antimicrobial Agents and Chemotherapy.
(Excerpt) Read more at eurekalert.org ...
Fascinating out-of-the-box thinking.
Probably coming just in time, if this pans out. I hope they can as well target certain bacteria to neuter just the bad guys.
Antibiotic therapy is the most commonly-used strategy to control infections of pathogens; however, it has contributed to the generation of antibiotic resistant bacteria. To circumvent this emerging problem, we are searching for compounds that target bacterial virulence factors rather than their viability. Pseudomonas aeruginosa, an opportunistic human pathogen, possesses a type III secretion system (T3SS) as one of its major virulence factors by which it secretes and translocates T3 effector proteins into human host cells. The fact that this human pathogen is also able to infect several plant species, led us to screen a library of phenolic compounds involved in plant defense signaling and their derivatives for novel T3 inhibitors. Promoter activity screening of exoS, which encodes a T3 secreted toxin, identified two T3 inhibitors and two T3 inducers of P. aeruginosa PAO1. These compounds alter exoS transcription by affecting the expression levels of the regulatory small RNAs RsmY and RsmZ. These two small RNAs are known to control the activity of a carbon storage regulator RsmA, which is responsible for the regulation of the key T3SS regulator ExsA. As RsmY and RsmZ are the only targets directly regulated by GacA, our results suggest that these phenolic compounds affect the expression of exoS through the GacSA-RsmYZ-RsmA-ExsA regulatory pathway.
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