Neutrophils play a critical role in the progression of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). ALI/ARDS are characterized by increased permeability of the alveolar-capillary barrier, leading to lung edema and impaired oxygenation. Neutrophils are among the first immune cells to migrate to the site of inflammation and contribute to tissue damage through the release of antimicrobial substances such as oxidants, proteinases, and cationic peptides. However, unregulated release of these substances can damage host tissues. Neutrophil recruitment into the lung is a key event in ALI, and their activation and transmigration are hallmarks of the disease. Neutrophils are involved in both the initial injury and the subsequent inflammatory response, which can lead to increased permeability and hyaline membranes. The mechanisms of neutrophil recruitment involve selectins, integrins, and chemokines, with selectins playing a role in the initial rolling of neutrophils on the endothelium. Integrins are involved in adhesion and transmigration of neutrophils into the lung tissue. Chemokines such as IL-8, CXCL1, CXCL2, and CXCL5 are important in recruiting neutrophils to the site of injury. Neutrophil-derived granule proteins, such as defensins and cationic polypeptides, contribute to tissue damage and inflammation. Additionally, neutrophil-derived serine proteases, including neutrophil elastase and cathepsin G, play a role in the pathogenesis of ALI by degrading surfactant proteins and increasing permeability. Matrix metalloproteinases (MMPs) also contribute to ALI by modulating inflammation and neutrophil influx. Reactive oxygen species (ROS) produced by neutrophils can cause oxidative damage to lung tissues. Overall, neutrophils are essential in the pathogenesis of ALI and ARDS, and their activity can be targeted for therapeutic intervention.Neutrophils play a critical role in the progression of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). ALI/ARDS are characterized by increased permeability of the alveolar-capillary barrier, leading to lung edema and impaired oxygenation. Neutrophils are among the first immune cells to migrate to the site of inflammation and contribute to tissue damage through the release of antimicrobial substances such as oxidants, proteinases, and cationic peptides. However, unregulated release of these substances can damage host tissues. Neutrophil recruitment into the lung is a key event in ALI, and their activation and transmigration are hallmarks of the disease. Neutrophils are involved in both the initial injury and the subsequent inflammatory response, which can lead to increased permeability and hyaline membranes. The mechanisms of neutrophil recruitment involve selectins, integrins, and chemokines, with selectins playing a role in the initial rolling of neutrophils on the endothelium. Integrins are involved in adhesion and transmigration of neutrophils into the lung tissue. Chemokines such as IL-8, CXCL1, CXCL2, and CXCL5 are important in recruiting neutrophils to the site of injury. Neutrophil-derived granule proteins, such as defensins and cationic polypeptides, contribute to tissue damage and inflammation. Additionally, neutrophil-derived serine proteases, including neutrophil elastase and cathepsin G, play a role in the pathogenesis of ALI by degrading surfactant proteins and increasing permeability. Matrix metalloproteinases (MMPs) also contribute to ALI by modulating inflammation and neutrophil influx. Reactive oxygen species (ROS) produced by neutrophils can cause oxidative damage to lung tissues. Overall, neutrophils are essential in the pathogenesis of ALI and ARDS, and their activity can be targeted for therapeutic intervention.