Research

Research Focus

Research in the PIIRL is focused on the resolution of inflammation and repair following lung injury. Lung injury, which leads to acute respiratory distress syndrome (ARDS), is characterized by profound inflammation, edema, and tissue injury often resulting from trauma or severe pulmonary infection. Although ARDS survival rates have improved in recent years, 25 to 40% of cases remain fatal, and of those patients that do survive, persistent inflammation and fibrosis can result in continued pulmonary complications.

Projects

Current projects include assessing the role of metalloproteinases and their endogenous inhibitors, the tissue inhibitors of metalloproteinases (TIMPs) in regulating three different aspects of recovery following lung injury: 1) microvascular endothelial cell dysfunction; 2) macrophage polarization and apoptosis; and, 3) initiation and resolution of fibrosis. Additional projects include examining the role of caspases and cell death in microvascular endothelial cell dysfunction during septic lung injury, as well as determining the effects of aging and exercise on the pathophysiology of lung injury. For these studies, we use multiple murine models of direct lung injury, including bleomycin (a model often used to study chronic lung injury and fibrosis) and Pseudomonas aeruginosa infection, as well as cecal ligation and perforation, a murine model of sepsis that results in indirect lung injury. Techniques such as flow cytometry, immunohistochemistry, quantitative real-time polymerase chain reaction, western blotting, and enzyme activity assays, in combination with culture of isolated primary cells, are then used to examine how specific cell populations are affected during lung injury.

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