# Restoring macrophage function in cystic fibrosis

> **NIH NIH R01** · OHIO STATE UNIVERSITY · 2020 · $312,000

## Abstract

Summary
This Administrative Supplement is in response to NOT-HL-19-724 (Notice of Special Interest (NOSI): Availability
of Administrative and Revision Supplements to Expand Vaping Research and Understand EVALI). ). The original
grant (5R01AI124121-04) is focused on understanding the role of the ion channel Cystic Fibrosis
Transmembrane conductance Regulator (CFTR) on exacerbated inflammation in the airways. Patients with
mutations in this ion channel leading to its malfunction develop Cystic Fibrosis (CF), a disease associated with
impaired bacterial clearance and increased lung inflammation, which ultimately results in lung failure. As an ion
channel, CFTR regulates fluid homeostasis in the lung. In addition, our published studies demonstrated for the
first time that macrophages lacking functional CFTR had impaired autophagy resulting in excessive inflammatory
profile. Relevant to this Supplement, findings from our group revealed that pollutants, such as cigarette smoke
and the psychoactive ingredient present in marijuana delta-9-tetrahydrocannabinol (THC), negatively regulate
CFTR leading to “acquired CFTR dysfunction”. In addition to inflammation, the CFTR ion channel plays also a
role in fluid homeostasis in the lung such as edema. Within the past few months, several people were hospitalized
and many died after developing lung disease linked to vaping: “e-cigarette, or vaping, product use-associated
lung injury” called EVALI which is characterized by excessive lung inflammation and pulmonary edema. We
therefore hypothesize that inhibition/decrease of CFTR function by THC and/or vitamin E acetate will contribute
to EVALI.
In Aim 1, we will determine the effect of the different agents present in vaping preparations associated with
EVALI on lung inflammation. Mice will be exposed to vaping preparations and a comprehensive assessment of
lung inflammation (multiplex, flow cytometry, RNAseq) will be performed. In Aim 2, we will establish the role of
the CFTR ion channel on EVALI-like phenotype. Here we propose to use a mouse model that expresses different
levels of CFTR (WT, Hets, and KO). CFTR activators will also be tested to evaluate their ability to reduce vaping-
induced lung inflammation.

## Key facts

- **NIH application ID:** 10116037
- **Project number:** 3R01AI124121-05S2
- **Recipient organization:** OHIO STATE UNIVERSITY
- **Principal Investigator:** Amal O Amer
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $312,000
- **Award type:** 3
- **Project period:** 2016-02-01 → 2021-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10116037

## Citation

> US National Institutes of Health, RePORTER application 10116037, Restoring macrophage function in cystic fibrosis (3R01AI124121-05S2). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10116037. Licensed CC0.

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