# Pulmonary Epithelial TRPV3 and Wood Smoke Injury

> **NIH NIH R01** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 2020 · $343,125

## Abstract

Project Summary/Abstract:
Combustion of wood and other forms of biomass releases enormous quantities of toxic materials into the air and
is linked to multiple human morbidities and an estimated 3-4M excess deaths/year. Like many forms of particulate
materials (PM), wood/biomass smoke PM (WBSPM) is pneumotoxic. WBSPM exposure increases people's
susceptibility to respiratory infections, exacerbates asthma, and causes emphysema and COPD. Exposure to
WBSPM is often unavoidable even in modern society and specific molecular and chemical interactions that link
exposure to the established acute and long term effects of WBSPM are not fully understood. Accordingly, the
ability to treat respiratory and other conditions resulting from exposure to WBSPM, and ways to effectively reduce
risks to humans, are extremely limited.
We propose a novel mechanistic paradigm for how WBSPM can cause deleterious effects in the lungs, through
activation of the Ca++ ion channel transient receptor potential vanilloid-3 (TRPV3). Our data show that WBSPM
activates TRPV3. Assessment of the proposed TRPV3-dependent mechanistic paradigm will provide
fundamental data to potentially predict human risks for respiratory conditions associated with WBSPM exposure
by establishing new mechanisms for toxicity. In doing so, this study has the potential to reveal innovative
approaches to discover interventions for the prevention and treatment of such diseases, and perhaps more
broadly, adverse effects caused by other pneumotoxins - based on indications that TRPV3 appears to play
fundamental roles in maintaining lung cell/tissue homeostasis during stress/after injury.
This study is motivated by results showing that TRPV3 is expressed by human lung epithelial cells, TRPV3 is
selectively activated by specific chemicals in PM obtained from burning multiple wood types, and this activation
is coupled to acute pro-inflammatory and pro-apoptotic signaling. Additionally, TRPV3 is dynamically regulated
and is involved in adaptive reprogramming of lung cells, sub-acute morphological changes in the airways of
mice, and compromised lung function. Our hypothesis is that TRPV3 plays dual roles in mediating both the acute
pro-inflammatory/cytotoxic effects of WBSPM as well as adaptation of lung cells to resist further damage to toxins
and airway remodeling. The specific aims are to: 1) further delineate the role of TRPV3 in acute and chronic
WBSPM pneumotoxicity; 2) decipher TRPV3, ER stress, COX2/PTGS2, and EGFR integration in lung injury and
repair; and 3) evaluate TRPV3 as a universal mediator of WBSPM toxicity.

## Key facts

- **NIH application ID:** 9870926
- **Project number:** 5R01ES027015-04
- **Recipient organization:** UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
- **Principal Investigator:** Christopher A Reilly
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $343,125
- **Award type:** 5
- **Project period:** 2017-03-01 → 2022-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9870926

## Citation

> US National Institutes of Health, RePORTER application 9870926, Pulmonary Epithelial TRPV3 and Wood Smoke Injury (5R01ES027015-04). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9870926. Licensed CC0.

---

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