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Cystic fibrosis breakthrough points to zinc as infection buster

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Cystic fibrosis breakthrough points to zinc as infection buster

Zinc has been found to be important in keeping lung infections at bay in people with cystic fibrosis, whose immune cell’s natural bacteria-fighting ability has been reduced by the genetic mutation that causes the disease. The discovery could result in treatments that reactivate the immune system, reducing infections.

The first ward I worked on as a brand-new registered nurse was the cystic fibrosis (CF) ward. Most of the patients were in their late teens and early 20s, many had recently transferred from the nearby Children’s Hospital. They both amazed and inspired me with their gritty determination and resilience in the face of what was, 25 years ago, a likely early death. While life expectancy has greatly improved since then, people with CF are still prone to complications resulting from the condition.

A mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene causes an excessive build-up of mucus in the lungs and dysregulated airway inflammation, making those with the condition susceptible to recurrent infections. Now, researchers from the University of Queensland (UQ), Australia, have identified a potential way of reducing infections in people living with CF, which hinges on zinc.

“People with CF 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,” said Peter Sly, a pediatric respiratory physician and co-author of the study. “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.”

Investigating how CFTR mutation affected the ability of immune cells called macrophages to fight off bacteria, the researchers found that, in CF, lung macrophages can’t properly use zinc as an anti-bacterial agent.

“One way that macrophages destroy bacteria is by poisoning them with toxic levels of metals such as zinc,” said Matt Sweet, the study’s corresponding author. “We discovered that the CFTR ion channel is crucial to the zinc pathway and because it doesn’t work properly in people with CF, it may partly explain why they’re more susceptible to bacterial infections.”

In addition to identifying the cells’ zinc dysfunction, the researchers also identified a zinc transport protein, SLC30A1, that restored the macrophage’s bacteria-killing ability in the context of CFTR mutation. Treatment with supplementary zinc was also sufficient to restore bacteria-killing in human lung macrophages in the lab.

The findings suggest that restoring the zinc toxicity response could be pursued as a therapeutic strategy to restore immune function and effective defenses in people with CF.

“Our goal is now to deliver this zinc transport protein to macrophages in people with CF with the expectation that it would reactivate their immune response and reduce infections,” Sweet said.

The study was published in the journal PNAS.

Source: UQ



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