IL1B and acute respiratory distress syndrome: The progress of ALI/ARDS is mainly driven by inflammatory response, evidenced by the activation of immune cells in ALI/ARDS, including macrophages, which secrete inflammatory mediators such as interleukin (IL)-1β, IL-6, IL-18, and tumor necrosis factor (TNF)-α, promoting the injury of alveolar epithelial cells and vascular endothelial cells [12,13,14,15,16,17].