# The Vagus Nerve in Lung Disease

> **NIH VA I01** · LOUISVILLE VA MEDICAL MEDICAL CENTER · 2020 · —

## Abstract

Pulmonary neuroendocrine (PNECs) cells are widely distributed throughout the
airway mucosa. These cells can be solitary or aggregated to form neuroepithelial
bodies (NEBs), which are richly innervated by the vagus nerve. PNECs/NEBs are
important for early phases of lung development and also associated with stem cell
niches in the airways. They are airway sensors. Airway sensory receptors are
biosensors that detect lung inflammation and injury through various mediators and
cytokines. This information is transmitted through vagal afferents to the brain and
produces a host of responses that regulate the pathophysiological process.
Increasing evidence suggests that the vagus nerve plays an important role in a
variety of pulmonary diseases from asthma, COPD, ARDS to lung cancer.
Pulmonary fibrosis (PF) can result from a variety of insults to the lung. Lung repair
following an insult-induced injury is a complex process involving both resident cells
and recruited cells. The progression of PF results from a network of interactions
among mediators, cytokines, and growth factors derived from inflammatory,
endothelial, and epithelial cells, which leads to lung remodeling, deposition of
collagen, limitation of gas exchange, and dyspnea. The vagus nerve is closely
related to each component of this network, thus its function may influence the
outcome of PF. Since lung injury is a major component in the development of PF
and harmful insults to the lung may stimulate the NEB-Vagal System (NVS), a novel
hypothesis that activation of the NVS promotes lung fibrosis will be tested. [If this
hypothesis is correct, suppression of the NVS should attenuate fibrosis, whereas
stimulation of the NVS should promote fibrosis. By examining lung fibrosis in
bleomycin treated mice in which the NVS is either stimulated or suppressed
(vagotomy, medication, gene manipulation, or cell adoptive transfer), and by
assessing well-established cellular and molecular pathways that lead to PF with
different techniques (histology, physiology, cytology and biochemistry), the
underlying neural mechanisms will be delineated.] Successful completion of the
studies will establish a novel neural mechanism in the pathogenesis of PF. [This
potentially may lead to a new pharmacological approach to treat or to limit chronic
fibrotic diseases in the Veteran population.]

## Key facts

- **NIH application ID:** 9898233
- **Project number:** 5I01BX003274-03
- **Recipient organization:** LOUISVILLE VA MEDICAL MEDICAL CENTER
- **Principal Investigator:** JERRY (Jun) YU
- **Activity code:** I01 (R01, R21, SBIR, etc.)
- **Funding institute:** VA
- **Fiscal year:** 2020
- **Award amount:** —
- **Award type:** 5
- **Project period:** 2018-04-01 → 2022-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9898233

## Citation

> US National Institutes of Health, RePORTER application 9898233, The Vagus Nerve in Lung Disease (5I01BX003274-03). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9898233. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*