This review summarizes recent advances in understanding the immunopathological mechanisms underlying sepsis-associated ALI, including macrophage polarization imbalance, excessive neutrophil extracellular trap (NET) formation, dendritic cell functional exhaustion, and dysregulation of key signaling pathways such as TLR4, NLRP3 inflammasome, and cGAS-STING. This evidence concerns the gene TLR4 and acute respiratory distress syndrome.