IL1B and acute respiratory distress syndrome: In the acute phase of ALI/ARDS, lung macrophages exhibit a predominant pro-inflammatory phenotype (M1), releasing a variety of potent pro-inflammatory and deleterious mediators such as tumor necrosis factor α (TNF-α), interleukin 1 (IL-1), nitric oxide (NO), and reactive oxygen species (ROS), all of which can cause an uncontrolled inflammatory response and excessive oxidative stress to damage the lung tissue.