Zinc deficiency increases risk of drug-resistant pneumonia

Not getting enough dietary zinc can increase the risk of a multidrug-resistant form of pneumonia that’s commonly seen in hospitals and nursing homes, according to a new study from University of Illinois Chicago researchers.  

Experiments led by Lauren Palmer, assistant professor of microbiology and immunology at UIC, found that zinc deficiency increased mortality in animals after they were infected with the bacteria Acinetobacter baumannii. The bacterial species is the second-leading cause of death from antimicrobial drug resistance worldwide. 

The researchers also discovered an allergy-like immune response in zinc-deficient animals after they were infected. This previously unobserved response could help clinicians prevent or treat pneumonia in hospitalized patients. 

The study published in Nature Microbiology shows how diet can affect susceptibility to infection and the severity of disease.

“Dietary deficiencies can contribute to being immunocompromised,” Palmer said. “By studying these environmental factors of infectious disease, we can potentially uncover underlying mechanisms that we can’t otherwise observe.” 

The study found that mice fed a low-zinc diet before they were exposed to A. baumannii had more bacteria in their lungs and other organs and higher mortality in the days following infection, compared with mice on a normal diet. Researchers traced the more severe outcomes to a key immune system protein, a cytokine called IL-13 related to inflammation and the body’s allergic response.  

“We had not looked at that factor before, because we don’t observe it being produced at high levels under normal diet conditions,” Palmer said. “By perturbing the system with the low-zinc diet, we uncovered a mechanism that may happen all the time.” 

Treating the low-zinc diet mice with an antibody against IL-13 reduced mortality and the spread of the bacteria after infection. Palmer said a similar drug has been tested as an immunotherapy in humans and found safe, meaning it could serve as a clinical protection against severe infection in zinc-deficient or high-risk people. 

“We saw that it eliminated the differences between the zinc-deficient and zinc-sufficient animals,” Palmer said. “If we can neutralize that IL-13 cytokine, then maybe that can help protect individuals from mortality and bacterial migration to other organs,” Palmer said. 

In addition to Palmer, the paper includes UIC co-authors Dziedzom Bansah, Xiaomei Ren and John Geary.