PPARG and Sepsis: In the mouse model of lipopolysaccharide- (LPS-) induced sepsis involving pulmonary inflammation and injury, endothelial cell PPARγ (ePPARγ) deficiency intensifies the tissue injury with increased pulmonary edema and capillary permeability, elevated ROS and cytokine/chemokine production, infiltration of neutrophils to the lungs, and expression of inflammation-associated adhesion molecules such as ICAM-1 and PECAM-1.