# The impact of dietary zinc deficiency on innate immunity to lung infection

> **NIH NIH R00** · UNIVERSITY OF ILLINOIS AT CHICAGO · 2022 · $86,722

## Abstract

Zinc deficiency is a major risk factor for pneumonia, and is estimated to contribute to 16% of
lower respiratory infections globally by the World Health Organization. Acinetobacter baumannii
is a leading cause of ventilator associated pneumonia and is a critically important opportunistic
pathogen due to its rising rates of multi-drug resistance. Patients at risk for hospital and
community acquired A. baumannii are also at increased risk of zinc deficiency. Our exciting
preliminary data show that zinc deficiency significantly increases mortality from A. baumannii
pneumonia by 24 h post infection, and that neutralization of the type 2 cytokine IL-13 protects
mice from mortality. These preliminary data form the basis of investigating the unknown
mechanisms linking zinc deficiency and pneumonia that will identify new therapeutic targets to
support immunity during lung infection of zinc deficient patients. The central hypothesis of this
proposal is that dietary Zn deficiency promotes type 2 inflammation during lung
infection, preventing A. baumannii killing by leukocytes. The research plan will identify
molecular mechanisms underlying the link between zinc deficiency and pneumonia. The
proposed experiments use an innovative multi-disciplinary approach to uncover potential
therapeutic targets to promote lung innate immunity during infection by a multi-drug resistant
organism. In order to determine the effect of Zn deficiency on leukocyte-mediated bacterial
killing, we will test the effect of zinc deficiency on leukocyte function using sophisticated animal
models and an engineered suite of fluorescent A. baumannii to probe the host-pathogen
interface. We will additionally identify the mechanism by which Zn deficiency promotes IL-13
production and pathogenic effects. Finally, we will determine the effect of Zn deficiency on the
lung epithelium in type 2 signaling and A. baumannii translocation. These aims were developed
independently and form the basis of my future research program to identify the molecular
mechanisms by which changes in host zinc metabolism affect susceptibility to the emerging
pathogen A. baumannii.

## Key facts

- **NIH application ID:** 10478314
- **Project number:** 3R00HL143441-04S1
- **Recipient organization:** UNIVERSITY OF ILLINOIS AT CHICAGO
- **Principal Investigator:** Lauren Disterhoft Palmer
- **Activity code:** R00 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $86,722
- **Award type:** 3
- **Project period:** 2021-02-01 → 2024-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10478314

## Citation

> US National Institutes of Health, RePORTER application 10478314, The impact of dietary zinc deficiency on innate immunity to lung infection (3R00HL143441-04S1). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10478314. Licensed CC0.

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