Consequently, in our study, we used the liver X receptor antagonist T0901317 (T0) to enhance the expression of LXRα and further verify the functions of LXRα in sepsis-induced lung tissue; further, we identified a novel mechanism by which LXRα regulated macrophage autophagy via the S100A8 signaling pathway, which we hope would serve as a novel target for treating ALI (Supplementary Figure S1). Here, NR1H3 is linked to acute respiratory distress syndrome.