University of Queensland researchers have identified an opportunity to reduce infections in people living with cystic fibrosis.

Researchers from the University of Queensland have discovered a fault in the bacteria-killing function of immune cells in people with cystic fibrosis and a potential way to get around it. The discovery offers an opportunity to reduce infections in people living with cystic fibrosis.

The study is published in Proceedings of the National Academy of Sciences.

Matt Sweet, PhD, in the University of Queensland’s Institute for Molecular Bioscience, says the team has found that, in people with cystic fibrosis, immune cells called macrophages are defective in a zinc pathway that the body uses to kill bacteria. 

“One way that macrophages destroy bacteria is by poisoning them with toxic levels of metals such as zinc,” Sweet says in a release. “We discovered that the CFTR (cystic fibrosis transmembrane conductance regulator) ion channel is crucial to the zinc pathway, and because it doesn’t work properly in people with [cystic fibrosis], it may partly explain why they’re more susceptible to bacterial infections.”

Importantly, the researchers also identified a zinc transport protein that can restore the macrophages’ ability to kill bacteria when the CFTR protein is not working.

“Our goal now is to deliver this zinc transport protein to macrophages in people with [cystic fibrosis] with the expectation that it would reactivate their immune response and reduce infections,” Sweet says in a release.

Around 3,600 Australians live with cystic fibrosis, which can reduce life expectancy to an average of 47 years.

Peter Sly, MD, at the University of Queensland’s Child Health Research Centre, a pediatric respiratory physician and key collaborator on the project, says discovering more about how cystic fibrosis affects the immune system is key to patient care.

“People with [cystic fibrosis] have a hyper-inflammatory state in their airways and are very susceptible to bacterial infections but frequent treatment with antibiotics can often lead to antibiotic-resistant infections,” Sly says in a release. “Current treatments can restore many aspects of CFTR function, but they don’t resolve or prevent lung infections. So there is a need to restore immune functions.”

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