Gill / Mehta Lab
Research in the Gill/ Mehta Lab is focused on understanding the mechanisms that regulate inflammation, tissue injury, and repair following lung injury, with a primary focus on indirect injury due to sepsis.
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:
- microvascular endothelial cell dysfunction;
- macrophage polarization and apoptosis; and,
- initiation and resolution of matrix remodelling.
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 septic lung injury.
For these studies, models utilizing cecal ligation and perforation, a murine model of sepsis that results in indirect lung injury, as well as multiple murine models of direct lung injury, including bleomycin (a model often used to study chronic lung injury and fibrosis) and Pseudomonas aeruginosa infection.
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.