Scientists say the findings offer hope in the battle against the rising number of drug-resistant infections
Some commonly used pain medications may have the ability to fight antibiotic-resistant infections caused by so-called “superbugs,” researchers said in a study published Thursday in scientific journal Chemistry & Biology.
Researchers at the University of Wollongong in Australia found that the anti-inflammatory painkillers – used for maladies such as arthritis and eye ailments in both humans and pets – have the secondary effect of preventing some bacteria from multiplying.
Drug-resistant infections have been blamed on the excessive use of antibiotics, resulting in the reduced effectiveness of many traditional drugs. Bacteria that were once easily killed by antibiotics have adapted to resist them, leaving doctors scrambling for treatment options.
Infections caused by drug-resistant bacteria hit about 2 million people in the U.S. each year, leading to at least 23,000 deaths, according to data from the U.S. Centers for Disease Control and Prevention (CDC).
Researchers said the drugs involved in the Australian study are non-steroid anti-inflammatory drugs, or NSAIDS, a class of medications that also includes aspirin and Ibuprofen.
“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,” the research report’s lead author, Associate Professor Aaron Oakley, said in a news release. “This is important because the superbugs have become resistant to many – and in some cases most – of the available antibiotics.”
The researchers tested three pain relievers used to treat various ailments in people and pets – bromfenac, carprofen and vedaprofen – and found that they all had the ability to inhibit replication among some bacteria.
The researchers said they found that the drugs acted on bacteria in a way that is fundamentally different from current antibiotics by binding to a part of a bacterium called a “DNA clamp,” preventing the organism from replicating or repairing its DNA and thus eventually killing it. Existing antibiotics work by disrupting the formation of a bacterium’s cell contents, but no current antibiotics target the DNA clamp, Oakley told Al Jazeera.
However, some experts said it is too early to know if the study’s findings will lead to a new class of antibacterial drugs. “I saw no compelling connection made between the biochemical activities that were observed and the antibacterial activity,” Richard H. Ebright, professor of chemistry and chemical biology at Rutgers University, told Al Jazeera.
But Oakley said the findings are a step in the right direction. “While our research is a long way from clinical trials, the fact that the bacteria-killing effects of the anti-inflammatories is different from conventional drugs means that they could be developed into new kinds of antibiotics,” he said in the news release.