NR1H3 and Sepsis: Acute lung injury involves intrapulmonary neutrophil accumulation and activation with the release of cytotoxic compounds, which leads to loss of the alveolar epithelial and capillary endothelial barrier function and increase in permeability of the alveolo-capillary membrane.18,19 In the present study, we used complementary pharmacological gain-of-function and genetic loss-of-function approaches to demonstrate that LXRα signaling is instrumental in modulating neutrophil infiltration in sepsis-induced lung injury.