We provide evidence of activation of IL-4 pathways in the setting of acute lung injury (ALI) and demonstrate that IL-4 prevents neutrophil hypoxic HIF-1α induction, abrogates hypoxic survival of human and mouse neutrophils, dampens proinflammatory cytokine expression, and promotes resolution of neutrophilic inflammation in vivo. This evidence concerns the gene IL4 and acute respiratory distress syndrome.