MANCHESTER, U.K.—You may have heard about drugs disappearing into people's noses. But at a meeting here this week and in a new paper, scientists presented the opposite: A new antibiotic that has, quite literally, emerged from the human nose. The compound is produced by one species of nose-dwelling bacterium to kill another microbe, which kills thousands of people every year.
The study is “yet another demonstration that we should look to nature for solutions to the problems nature throws at us,” says Andrew Read, an evolutionary biologist at Pennsylvania State University, University Park, who was not involved with the work.
Any new antibiotic is welcome because the world is running out of these life-saving drugs. But the researchers behind the new finding believe that studying the microbial warfare going on inside our bodies may lead to not just one, but a whole slew of novel drugs. “We’ve found a new concept of finding antibiotics,” Andreas Peschel, a bacteriologist at the University of Tübingen in Germany, said on Tuesday at the EuroScience Open Forum, a biennial science and policy meeting. “We have preliminiary evidence at least in the nose that there is a rich source of many others, and I’m sure that we will find new drugs there.”
Peschel and bacteriologist Bernhard Krismer, also at the University of Tübingen, started out investigating why roughly every third person carries a bacterium called Staphylococcus aureus in their nose. Most of the time, S. aureus is harmless, but occasionally, it causes severe, even life-threatening, disease—for instance when it gets into an open wound and causes sepsis. S. aureus is a notorious hospital dweller, and its drug-resistant form, known as MRSA (for methicillin-resistant Staphylococcus aureus) is a major public health problem, killing more than 10,000 people a year in the United States alone.
But why do some people carry S. aureus in their nose, whereas others don't? Analyzing human nasal secretions—also known as snot—Peschel and Krismer found that the nose is not a very hospitable niche for microbes. “If I were a bacterium I would not go into the nose,” Peschel says. “There is nothing there, simply a salty liquid and a tiny amount of nutrients.”
Those harsh conditions might lead to fierce competition for resources, the researchers reasoned. So they tested what effect a collection of other Staphylococcus species had on S. aureus. One bacterium, S. lugdunensis, turned out to be very good at preventing S. aureus from growing. The researchers found that the bacterium produced an antibiotic compound and succeeded in synthesizing it in the laboratory. The chemical, which they named lugdunin, inhibited S. aureus from growing in the petri dish, and when applied to the skin of mice infected with S. aureus, it reduced or even eradicated the infection, the team reports today in Nature. It was also effective against antibiotic-resistant strains like MRSA.
Just how lugdunin works is unclear. The researchers say that S. aureus did not evolve resistance to it, however, even when exposed to low levels over a period of 30 days.
The scientists then analyzed the microbial populations in the noses of 187 hospitalized patients. Sixty of them carried S. aureus and 17 S. lugdunensis; only one patient carried both. That suggests S. lugdunensis is a powerful enemy of S. aureus, the authors say.
“This is extremely exciting as it provides evidence that a microbial war is ongoing in our body,” says Jack Gilbert, a microbial ecologist at the University of Chicago in Illinois. On a practical level, he says, the research shows “that certain organisms can be leveraged to create novel drugs that could add to our arsenal of weapons against drug-resistant [microbes].”
But using such new weapons may have unintended consequences, warns Peer Bork, a computational biologist at the European Molecular Biology Laboratory in Heidelberg, Germany. “Yes, it’s a cool finding,” he says. But the microbiome is a delicate balance that has evolved over millions of years, he cautions. “It’s more complex than goodies and baddies. Tinkering around might destroy long-evolved community relations.”
Peschel does not see any big risks, however. “S. aureus is really the most important pathogen that colonizes human noses,” he says, so if lugdunin could get rid of it, it would be hard to imagine a negative outcome. Theoretically, instead of using the antibiotic, you could also allow S. lugdunensis to colonize patients at risk from S. aureus, he says—a probiotics treatment for the nose. The problem is that S. lugdunensis is itself associated with a range of infections—including of the heart, joints, skin, and eyes—so that strategy could be dangerous. “There may be other bacteria where that is an option,” Peschel says.
Read is skeptical of claims that lugdunin may not trigger resistance, because every antibiotic developed so far has run into resistance problems. “Antibiotic use that does not drive resistance is the holy grail,” he says. “Fantastic if lugdunin turns out to be one such case. But history tells us not to hold our breath.”