A clinical study concerning anti-cancer agents has found that certain pathogens can escape the most potent drugs by sacrificing themselves, demonstrating a possible new form of antibiotic resistance.
Adding to the collection of strategies scientists have already discovered and studied, this discovery shows that dangerous microbes are continuing to develop new means of evading destruction by antibiotics.
The new method of antibiotic resistance was published in last week’s edition of the journal Science.
Jon Thorson, a University of Wisconsin professor of pharmacology, is the senior author of the paper. Thorson’s team of UW researchers conducted the work cited in the paper.
“It is a new paradigm. It shows that bacteria are still finding new mechanisms to resist our antibiotics,” Thorson said.
Scientists have known for a long time that bacteria can evade antibiotics by changing their chemistry, keeping prescribed drugs from binding to the parasitic cell.
One way in which bacteria resist the potency of antibiotics is to pump out the drug that has invaded the affected cell. Scientists have also learned that microbes can make proteins that bind to the drug and put it out of circulation before it can do its work.
“This could possibly become another category, depending on how often [this mechanism] is found,” Thorson said.
The discovery was made while using enediyne, a highly potent anti-cancer agent. Enediynes are naturally occurring anti-tumor antibiotics that work by tearing up DNA and upsetting a cell’s ability to reproduce and function, therefore destroying cells such as cancer.
Bacteria in nature sometimes use enediynes to create an area free of other microbes, but since this environment is so toxic, the microbe must find a way to survive in the poison it creates.
As Thorson said, if a bacterium soaks up some of its own toxin, it then protects itself by deploying a protein that intercepts the enediyne before it destroys the organism’s DNA. The enediyne leaves the protein instead of the DNA, but the organism inactivates itself by deploying the protein.
“It’s somewhat inefficient, but at least the cell survives,” Thorson said.
While this reaction was found only in this specific study, Thorson said that many drugs are coming from bacteria such as the enediyne-producing bacteria.
Thorson said the results of the study are not applicable to the world of medicine at the moment. Before any hype is made out of the discovery, more studies must be done to see if this resistance mechanism pops up in cases other than this certain bacterium.
“We’re now trying to understand what the genes do in making the enediyne,” Thorson said.
Once this is determined, scientists could alter the chemistry by removing the certain gene and using it to advance the field of cancer-treatment research.
