A new study published in Nature Microbiology reveals that dietary zinc deficiency significantly increases the risk of lung infections caused by Acinetobacter baumannii, a leading cause of ventilator-associated pneumonia. The research, led by a team at Vanderbilt University Medical Center, establishes a novel connection between the pro-inflammatory cytokine interleukin-13 (IL-13) and A. baumannii infections, demonstrating that blocking IL-13 can prevent infection-related mortality in animal models.
The study suggests that FDA-approved anti-IL-13 antibodies may offer protection against bacterial pneumonia in patients suffering from zinc deficiency. “To our knowledge, this is the first study to show that neutralizing IL-13 can prevent death from a bacterial infection,” said Eric Skaar, PhD, MPH, the Ernest W. Goodpasture Professor of Pathology and director of the Vanderbilt Institute for Infection, Immunology and Inflammation. “This discovery opens the door for personalized therapy approaches using anti-IL-13 treatments in patients with zinc deficiency and A. baumannii pneumonia.”
Globally, nearly 20% of the population is at risk for zinc deficiency, which can weaken immune responses and significantly heightens the risk of pneumonia. The World Health Organization identifies zinc deficiency as a major contributor to disease and mortality. Individuals at heightened risk include critically ill and elderly patients, particularly those in healthcare settings, such as intensive care units or those requiring ventilators and catheters. A. baumannii infections are becoming increasingly resistant to antimicrobial treatments, posing a significant public health challenge.
To investigate the role of dietary zinc deficiency in A. baumannii pathogenesis, the researchers developed a mouse model simulating both zinc deficiency and acute A. baumannii pneumonia. Led by Lauren Palmer, PhD, a former postdoctoral fellow at VUMC now at the University of Illinois, Chicago, the study found that zinc-deficient mice exhibited a higher bacterial load in the lungs, increased spread of bacteria to the spleen, and greater mortality rates compared to their zinc-sufficient counterparts.
The researchers observed that zinc-deficient mice produced elevated levels of IL-13 during infection, and introducing IL-13 to mice with adequate zinc levels facilitated the spread of A. baumannii to the spleen. Notably, treatment with anti-IL-13 antibodies protected zinc-deficient mice from death caused by A. baumannii.
These findings contribute to a growing body of research linking nutrient deficiencies to increased IL-13 production and a “type 2” immune response, suggesting that IL-13 may be a critical factor in healthcare-associated and opportunistic lung infections. “This further supports the exploration of IL-13 as a therapeutic target,” Skaar noted.
The FDA-approved anti-IL-13 antibodies, lebrikizumab and tralokinumab, have been extensively studied as potential treatments for uncontrolled severe asthma. While they did not prove effective for that indication, clinical trials confirmed their safety.
Palmer and Skaar are co-corresponding authors of the Nature Microbiology report, which also includes contributions from Zachery Lonergan, PhD, Dziedzom Bansah, Xiaomei Ren, PhD, Lillian Juttukonda, MD, PhD, Christopher Pinelli, DVM, PhD, and Kelli Boyd, DVM, PhD. The research received partial funding from the National Institutes of Health through various grants.
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