A new study, published in mBio, exposes a zinc-import system in bacteria that could contribute to their ability to cause infection.

The study looked at how the bacterium Staphylococcus aureus, which can infect virtually all of the tissues in the human body, competes with the immune system for the essential nutrient zinc.

“Transition metals such as zinc are essential for all forms of life,” said Thomas Kehl-Fie, professor of microbiology. “We get these metals from food, while invading bacteria must get them from us.”

In order to combat an infection, the body’s immune system hoards zinc and other critical nutrients, in an effort to weaken the bacteria. “The host and bacteria are, in effect, engaged in a tug of war for zinc,” said Kehl-Fie. “Our immune system tries to remove zinc from sites of infection and the bacteria, while the bacteria use transporters to pull the metal away from the host.”

Kehl-Fie and colleagues discovered a new system that enables S. aureus to acquire zinc from the human body. The discovery explains how S. aureus is able to grow well even in environments that are very zinc-limited.

“The system we identified represents a new class of zinc transporters. Differing from other zinc transporters, it uses a secreted metal-binding molecule called a metallophore. While metallophores are known to enable bacteria to obtain iron during infection, this is the first example of a bacteria using this strategy to obtain zinc from the host,” said Kehl-Fie.

Kehl-Fie's lab in collaboration with a team at the Carl R. Woese Institute for Genomic Biology to discovered that analogous transporters are present in other pathogens as well.

The metallophore molecule can import zinc into the bacteria even when the amount of zinc in the environment is extremely low. This means that, even with the immune system acting in full-force against these bacteria, they can still obtain this essential nutrient in the human body.

“This discovery not only means we know more about how these bacteria infect the human body, but could open up new ways to help fight infection of this type,” said Kehl-Fie.

“The continued emergence and spread of antibiotic resistance highlights the need for new therapeutics to treat bacterial infections,” he said.

Graduate student Kyle Grim was the lead author of the paper. The Kehl–Fie lab is supported by the NIH, March of Dimes, and the Vallee Foundation. The Department of Microbiology is part of the School of Molecular and Cellular Biology.