Zinc has been found to be important in preventing lung infections in individuals with cystic fibrosis, as their immune cells' ability to fight off bacteria is reduced due to the genetic mutation that causes the disease. This discovery could lead to treatments aimed at reactivating the immune system, thereby reducing inflammation. According to an article published on New Atlas, citing the PNAS journal, cystic fibrosis, which was associated with potential early death 25 years ago, has seen significant improvements in life expectancy since then; however, individuals with cystic fibrosis remain susceptible to complications arising from the condition.
A mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene causes excessive mucus accumulation in the lungs and uncontrolled airway inflammation, making affected individuals prone to recurrent infections. Researchers from the University of Queensland in Australia have discovered a potential method to reduce infections in people with cystic fibrosis, which relies on zinc.
Peter Sly, a pediatric respiratory physician and co-researcher in the study, stated, "Individuals with cystic fibrosis experience severe airway inflammation and are more susceptible to bacterial infections, but repeated antibiotic treatments often lead to antibiotic-resistant infections." Dr. Sly added, "Current treatments can restore many aspects of CFTR function, but they do not resolve or prevent lung infections, indicating the need to restore immune functions."
By studying how the CFTR mutation affects the immune cells known as macrophages in fighting bacteria, the researchers found that in cystic fibrosis, pulmonary macrophages are unable to properly utilize zinc as an antibacterial agent. Co-researcher Matt Sweet noted, "One way macrophages destroy bacteria is by poisoning them with toxic levels of minerals like zinc," emphasizing that "the CFTR ionic channel is essential for the zinc pathway, and since it does not function properly in cystic fibrosis patients, this partially explains why they are more prone to bacterial infections."
In addition to identifying the zinc dysfunction in the cells, the researchers also discovered the zinc transporter protein, SLC30A1, which restored the ability of macrophages to kill bacteria within the context of the CFTR mutation. This means that zinc supplementation treatment was also sufficient to restore bacterial killing in human lung macrophages in laboratory settings.
The findings suggest that restoring the response to zinc toxicity could be pursued as a therapeutic strategy to restore immune function and effective defenses in individuals with cystic fibrosis. Researcher Sweet explained that the current goal is "to deliver the zinc transporter protein to macrophages in individuals with cystic fibrosis, expecting it to reactivate their immune response and reduce infections."
