Pulmonary fibrosis, a form of interstitial lung disease, is a leading cause of death in Systemic Sclerosis (SSc). Recent work has suggested that lung macrophages play a key role in its development in SSc patients. Lung transplants performed on these patients provide a unique opportunity to study these cells on the molecular level in both the healthy donor and explanted fibrotic lung. We propose to use genomic assays to compare the regulatory networks of lung macrophages from SSc with healthy individuals. We will also examine the variability in macrophage regulation across fibrotic lungs. Through computational analysis, we can implicate molecular regulators and environmental signals that reprogram the macrophage networks. This project will provide an important resource for lung disease and inform on the applicability of mouse models for fibrosis. These results will offer a better understanding of the fibrotic environment and will likely lead to specific targets for therapy.
|Effective start/end date||7/1/17 → 6/30/20|
- American Lung Association (DA-514725)