UW Pulmonary, Critical Care and Sleep Medicine
Email: email@example.com | Phone: 206.543.3166
My main interest is to understand the mechanisms leading to alveolar epithelial damage in acute lung injury, and the interactions of those mechanisms with lung host defenses. We have focused primarily on the role of apoptosis in the development of epithelial damage, with a particular emphasis on the Fas/FasL system. Our current hypothesis is that the Fas/FasL system plays multiple roles in the pathogenesis of acute lung injury, depending on the target cell: it contributes to destruction of the epithelium by promoting apoptosis of alveolar epithelial cells, it contributes to the fibrotic response by promoting fibroblast proliferation and collagen deposition, and it contributes to the inflammatory response by promoting cytokine release from alveolar macrophages. We are approaching this hypothesis by combining genomic and proteomic analyses, molecular biology techniques, cell biology, and experimental models of lung injury.