Project 3: Mechanisms of alveolar epithelial apoptosis during acute lung injury

Approximately 200,000 people in the United States develop acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) annually (1). Despite research driven advances in therapy, 30%-40% of these patients will die. ALI and ARDS often manifest as a part of a systemic inflammatory process resulting in the development of diffuse alveolar epithelial damage and capillary injury with the exudation of protein rich fluid into the alveolar space. Influenza virus infects alveolar epithelial cells and causes ALI and ARDS. We are currently interested in examining the metabolic requirements of influenza viral replication in vitro and in vivo. Furthermore, we are testing whether mitochondrial dysfunction in epithelial cells worsens the responses to influenza in mice. Since aging results in mitochondrial dysfunction and is a risk factor for influenza induced lung injury, our studies will unravel the relationship between metabolism and influenza virus.

Mechansims of TGF-Beta induced apoptosis in epithelial cells.

Faculty

Navdeep S Chandel, Project Leader
Scott G. R. Budinger, Co-Leader