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New Study: Common Pain Relievers Fight Bacterial Infections

Mar 17 2014, 12:01am CDT | by

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New Study: Common Pain Relievers Fight Bacterial Infections
 
 

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New Study: Common Pain Relievers Fight Bacterial Infections

Potentially huge news is simmering in the world of infectious disease treatment. Researchers publishing in the journal Chemistry and Biology have found that common anti-inflammatory pain relievers could be a new weapon in the fight against antibiotic-resistant bacteria—ominously known as “superbugs.”

Regular antibiotics, like penicillin and amoxicillin, are targeted poisons designed to kill various forms of bacteria that make us sick. Some antibiotics accomplish this by destroying the bacterium’s ability to reproduce, others by interfering with the ability to turn blood glucose into energy, and still others by rupturing bacterial cell walls.

While genius drugs, the problem with antibiotics is that bacteria eventually mutate around their effects. When that happens, a new strain of antibiotic-resistant bacteria emerges, such as MRSA (Methicillin-resistant  Staphylococcus aureus ), resulting in tenacious infections that are difficult and sometimes impossible to treat. Many epidemiologists believe that chronic overuse of antibiotics is spawning these superbugs.

The latest research shows that common non-steroidal anti-inflammatory drugs (better known as NSAIDs) act on bacteria in a way that is entirely different than antibiotics—by binding to a specific protein in bacteria called the DNA Clamp, a key to bacterial multiplication.

“We discovered that some anti-inflammatory drugs used in human and veterinary medicine have weak antibiotic activity and that they exert this secondary activity by preventing bacteria from copying their DNA, which they need to do in order to multiply,” explains senior author Dr. Aaron Oakley of the University of Wollongong, in Australia.

The NSAIDs tested in this study were bromofenac (used to treat eye pain related to cataracts), carprofen and vedaprofen (both used by veterinarians to treat pain in dogs and horses).  The study didn’t include the most common NSAIDs, such as ibuprofen, naproxen and aspirin, but it’s possible that these drugs could have a similar effect.

All NSAIDs reduce pain and inflammation by blocking enzymes called Cox-1 and Cox-2 that make chemical compounds called prostaglandins. When we’re injured, prostaglandins are released by the damaged tissue causing swelling and intensification of nerve signals in the injured area (commonly known as pain). By blocking Cox-1 and Cox-2, NSAIDs reduce prostaglandin’s effects.

For reasons that aren’t yet clear, it appears that NSAIDs also act as blockers of the bacterial DNA Clamp, at least marginally. If these effects can be harnessed and amplified, modified versions of common pain relievers could eventually become a silver bullet in the fight against superbugs.

“The fact that the bacteria-killing effect of the anti-inflammatory drugs is different from conventional drugs means that the NSAIDs could be developed into new kinds of antibiotics that are effective against so-called superbugs,” says Dr. Oakley. “This is important because the superbugs have become resistant to many—and in some cases most—of the available antibiotics.”

Don’t run out to stock up on NSAIDs just yet. This study is just the start of what will likely be a lengthy round of research into how these drugs affect bacteria, and presently there is no solid scientific ground for attempting to treat bacterial infections with NSAIDs—although they are often effective at reducing fever associated with infections.

Having said that, this is exciting research with terrific promise in the ever-intensifying war against the superbugs.

The study was published online in the Cell Press journal Chemistry and Biology.

You can find David DiSalvo on Twitter @neuronarrative and at his website, The Daily Brain. His latest book is Brain Changer: How Harnessing Your Brain’s Power To Adapt Can Change Your Life.

Source: Forbes

 

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<a href="/latest_stories/all/all/31" rel="author">Forbes</a>
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