My training as a physician scientist motivates me to seek new treatments for chronic lung diseases. I have spent more than 15 years pursuing this goal by studying the relationship mechanisms of fibrotic remodeling in the adult mammalian lung. My laboratory has had a sustained impact on the field of pulmonary fibrosis and is credited with several seminal discoveries that have been verified and reproduced in laboratories around the world. My early work helped ignite interest in the mechanism(s) through which innate immunity is linked to pulmonary fibrosis. For example, my lab was the first to report that monocytes from patients with Scleroderma associated lung fibrosis adopt profibrotic properties following DAMP stimulation. We reported that the lungs of mice exposed to fibrotic stimuli, and humans with IPF, contain aberrantly activated macrophages that can be repolarized with innate immune agonists to attenuate experimentally induced lung fibrosis. We also are credited with linking intracellular DNA sensors and their ligands with numerous forms of interstitial lung disease. Most recently we reported that a previously unrecognized nerve-lung connection drives mammalian lung fibrosis. My work has been published in journals such as Science, Science Translational Medicine, Nature Medicine, Cell, Journal of Clinical Investigation, Lancet Respiratory Medicine, and the American Journal of Respiratory and Critical Care Medicine. I have been a continuous recipient of NIH funding since 2005 in the form of K08, R01 and U01 awards, and have been honored by my peers with the Jo Rae Wright Award from the American Thoracic Society and induction into the American Society of Clinical Investigation (ASCI). My discoveries in these domains have been informed by collaborations with Yale immunologists, neuroscientists, and bioengineers with the goal of developing new ways to improve respiratory health.