The long-term goal of our research is to define how innate immune responses activated in sepsis can be modulated to maximize protection and minimize tissue damage, thereby identifying potential therapeutic targets for prevention and treatment of sepsis. Our research has focused on acute lung injury, innate immunity and inflammation, and vascular endothelial permeability. We have established a record of successful and productive research in the areas highly relevant to lung inflammatory injury.
Project 1. Alveolar macrophages in lung inflammation and resolution. Like other tissue resident macrophages, alveolar macrophages display distinct and even sometime opposite abilities to initiate immune responses or to promote the resolution of lung inflammation. We will investigate how microenvironmental signals regulate the homeostatic renewal of alveolar macrophages during the pathogenesis and resolution of lung inflammation.
Project 2. Vascular endothelial barrier function. Vascular hyperpermeability and protein-rich edema resulted from disruption of the endothelial barrier is a key hallmark of inflammation. We will elucidate the signaling mechanisms that regulate endothelial permeability in response to inflammatory insults.
YAP Controls Endothelial Activation and Vascular Inflammation Through TRAF6
Rab11a Mediates Vascular Endothelial-Cadherin Recycling and Controls Endothelial Barrier Function