The research focus of my laboratory is to identify susceptibility factors and candidate pathways relevant to host biological responses to environmental pollutants. By carefully dissecting these links, we will gain insight into how environmental pollutants acutely induce respiratory symptoms and exacerbate chronic lung diseases. This can lead to targeted therapeutics and/or identify susceptible populations.
The central hypothesis of my research is that macrophages are key regulators of the biologic responses to environmental pollutants and the development of pulmonary fibrosis. My laboratory has pioneered the identification of novel pulmonary macrophage subsets and has defined their function in lung injury and repair. In both published work and areas of active investigation, we have identified macrophage subsets with unique genetic programming and function after challenges with environmental exposures such as ozone, wood smoke and silica. Since macrophages have both detrimental and protective functions, identifying these subsets offers the opportunity to understand their unique programing and function. This could allow development of targeted therapeutics that take advantage of these functions, polarize the immune responses and alleviate respiratory disease.
Education and Training
- Fellowship, Pulmonary And Critical Care, Duke University School of Medicine, 2006 - 2010
- Resident, Internal Medicine, Boston University, 2002 - 2006
- M.D., University of Tennessee, Memphis, 2002
- CXCL10/CXCR3 regulation of ozone-induced epithelial permeability
- Gene-Environment Collaboration in Autoimmune Disease
- GA39831: An observational study to assess disease relevant outcomes using home monitoring devices in patients with idiopathic pulmonary fibrosis
- Interdisciplinary Training Program in Lung Disease
- VTEU Task Order 16-0058 - Task C
- Using MRI To Visualize Regional Therapy Response In Idiopathic Pulmonary Fibrosis
- Dual humanization to model gene-environment interactions in ANCA vasculitis