Bronchopulmonary dysplasia (BPD) is a chronic lung disease caused by long periods of time spent on breathing machines or given supplemental oxygen in premature infants.
My areas of research revolve around bronchopulmonary dysplasia, bronchiolitis obliterans and rare lung diseases. Specifically, I’m looking at epithelial mesenchymal interactions in lung development, fibrosis and injury repair.
The goals of my lab are to better understand and uncover the molecular and cellular processes involved in the pathological injury response, which help us identify new targets for potential therapies.
My early research looked at the mouse lung epithelium. I generated the widely used, and extremely successful, tetracycline inducible system to either activate or inactivate genes within this lung epithelium. Additionally, in 2005, I created a transgenic mouse model to activate and inactive genes in the bronchiolar epithelium.
This model has been comprehensively used in my lab to delete and alter gene expression in the tracheal and bronchial epithelium to uncover their role in lung development as well as lung injury and repair. Expanding on this work, I’ve been branching out into researching fibrotic lung diseases, such as interstitial pulmonary fibrosis (IPF) and lymphangioleiomyomatosis (LAM).
I had two seminal first-author publications during my PhD training about the role of cell adhesion in tumor progression —both continue to be cited frequently.
The American Lung Association (2009-2011) funded my research to study pulmonary fibrosis. My colleagues and I studied how acute epithelial injury triggers loss of established lung allograft tolerance and leads to bronchiolitis obliterans (BOS). We have also used a transgenic mouse model to study the soluble dominant-negative FGF receptor (dnFGFR) during the prenatal period. The results showed reduced alveolar septae formation and subsequent alveolar simplification, which recapitulated some features of BPD in premature infants.
I have more than 20 years’ experience in the field of lung development and injury repair, and I initially joined the Cincinnati Children’s Hospital team in 1999. In 2010, I received the Carol Basbaum Award from the Respiratory Cell and Molecular Biology (RCMB) assembly in recognition of outstanding scientific achievement and leadership potential given to a junior investigator in the field of Respiratory Cell and Molecular Biology. I also received the Lymphangioleiomyomatosis (LAM) Established Investigator award in 2019 and was awarded the LAM Patient Benefit Grant in 2018.