Arthritis drug reinforces our last line of defense against superbugs

A virus might be the boogeyman of 2020, but we shouldn’t ignore bacteria as a looming health threat. The growing problem of antibiotic resistance isn’t slowing down, which could soon render our best drugs useless against infection. Now, researchers at the University of Hong Kong have found that an existing rheumatoid arthritis drug can be repurposed to cancel bacteria’s resistance to antibiotics.

Antibiotics were one of the most important scientific discoveries of the 20th century, but unfortunately decades of overuse has now caught up with us. Bacteria have evolved resistance to almost every drug we can throw at them, and if the problem isn’t addressed we could be headed into a new “dark age” of medicine, where even the most basic of infections becomes lethal once again.

To help prevent that nightmare scenario from coming to pass, the researchers on the new study investigated existing drugs that could turn the tide. The team found that auranofin, a drug used to treat rheumatoid arthritis since the 1980s, can restore the bacteria-killing function of two “last resort” antibiotics that are becoming ineffective.

Carbapenems are a class of antibiotics that are used to treat infections that are resistant to basically everything else in our arsenal. Colistin, meanwhile, is considered a last-last resort due to its severe side effects. Worryingly, bacteria are increasingly exhibiting resistance to both carbapenems and colistin.

In the new study, the researchers exposed multidrug-resistant E. coli to auranofin, and found that the drug inhibited two key enzymes that bacteria use to resist antibiotics. The first are called metallo-β-lactamases (MBLs), which bacteria use to break down carbapenems. The second is the mobilized colistin resistance (MCR) enzyme, which of course fights colistin.

When the team combined auranofin with either colistin or a carbapenem called meropenem, the team found that not only did the old drugs begin to kill the superbugs again, they could do so at a dose some 32 to 64 times lower than usual. That in turn could reduce some of the side effects.

In tests in mice with drug-resistant infections, the researchers found that combining auranofin and colistin killed 10 times more of the bacteria in the animals’ livers and spleen than just the antibiotic alone. Even better, in mice with a system-wide infection of an E. coli superbug, every single treated animal survived after a five-day treatment regime of auranofin and colistin.

While much more work needs to be done, including conducting tests in humans, the results so far are intriguing. This kind of treatment could help reinforce our last line of defense against superbugs, buying us more time to develop brand new antibiotics or other treatments.

The research was published in the journal Nature Communications.

Source: University of Hong Kong