Neutrophil-mediated lung injury may result from one or more of the following possible causes: 1) loss of the normal mechanisms that regulate and switch off neutrophil influx, 2) inappropriate or uncontrolled neutrophil activation within the lung, 3) inhibition of neutrophil apoptosis, and 4) impairment or saturation of the normal macrophage-dependent process for the removal of apoptotic neutrophils. Current in vitro data indicate that many factors operating at the inflamed site (e.g. cytokines, growth factors, chemotactic peptides, hypoxia, acidosis, etc.) serve a dual function in both priming and activating these cells, and delay apoptosis. The observation that the rate of eosinophil apoptosis can be accelerated by corticosteroid therapy in vivo suggests a novel mode of action for this drug and indicates that targeting this process in other granulocyte-dependent inflammatory conditions may offer a novel therapeutic approach in inflammatory lung disease.