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Zinc deficiency is associated with an increased risk of lung infections
Last reviewed: 02.07.2025

Dietary zinc deficiency contributes to the development of lung infection caused by Acinetobacter baumannii bacteria, which is a leading cause of ventilator-associated pneumonia, according to a new study published in the journal Nature Microbiology.
A team of researchers led by Vanderbilt University Medical Center has discovered an unexpected link between the proinflammatory cytokine interleukin-13 (IL-13) and A. baumannii lung infection and showed that blocking IL-13 prevents infection-related death in an animal model.
The study results suggest that anti-IL-13 antibodies approved by the FDA for use in humans may protect against bacterial pneumonia in patients with zinc deficiency.
"To our knowledge, this is the first study to show that neutralizing IL-13 can prevent mortality from bacterial infection. This finding suggests the potential for using anti-IL-13 therapy in zinc-deficient patients with A. baumannii pneumonia as part of a personalized treatment approach," said Erik Skaar, PhD, MPH, the Ernest W. Goodpaster Professor of Pathology and director of the Institute for Infection, Immunology, and Inflammation at Vanderbilt University.
Nearly 20% of the world's population is at risk of zinc deficiency, which can impair immune function and is a major risk factor for pneumonia. The World Health Organization considers zinc deficiency to be a leading contributor to disease and death.
Patients at risk for zinc deficiency, especially the seriously ill and elderly, are also at risk for A. baumannii infection. Patients in health care settings are at greatest risk, especially those on ventilators, with catheters, or in intensive care for long periods. A. baumannii is becoming increasingly resistant to antimicrobials, making it a serious public health threat, Skaar said.
To investigate whether and how dietary zinc deficiency contributes to the pathogenesis of A. baumannii, the researchers developed a mouse model of dietary zinc deficiency and acute A. baumannii pneumonia. The study was led by Lauren Palmer, PhD, a former postdoctoral fellow at VUMC and now an assistant professor in the Department of Microbiology and Immunology at the University of Illinois at Chicago.
The researchers found that zinc-deficient mice had increased bacterial loads in the lungs, bacterial dissemination to the spleen, and higher mortality compared with mice with adequate dietary zinc. They showed that zinc-deficient mice produced more IL-13 during infection, and that administering IL-13 to zinc-deficient mice promoted dissemination of A. baumannii to the spleen. Treatment with anti-IL-13 antibodies protected zinc-deficient mice from A. baumannii-induced death.
These findings add to a growing body of research showing that certain nutrient deficiencies are associated with IL-13 production and type 2 immune response.
"IL-13 may be an important risk factor for healthcare-associated pulmonary infections and opportunistic infections, highlighting the need for further exploration of IL-13 as a target for treatment," Skaar noted.
FDA-approved anti-IL-13 antibodies (lebrikizumab and tralokinumab) have been widely studied as potential treatments for uncontrolled severe asthma. Although they have not proven effective for this indication, clinical trials have shown them to be safe.