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Oxygen, which is widely used in neonatal medicine, constitutes one possible contributing neurotoxic factor, because it can trigger neuronal apoptosis in the developing brain of rodents. We hypothesized that two caspase\u20101\u2013processed cytokines, interleukin (IL)\u20131\u03b2 and IL\u201018, are involved in oxygen\u2010induced neuronal cell death. Six\u2010day\u2010old Wistar rats or C57\/BL6 mice were exposed to 80% oxygen for various time periods (2, 6, 12, 24, and 48 hours). Neuronal cell death in the brain, as assessed by Fluoro\u2010Jade B and silver staining, peaked at 12 to 24 hours and was preceded by a marked increase in mRNA and protein levels of caspase 1, IL\u20101\u03b2, IL\u201018, and IL\u201018 receptor \u03b1 (IL\u201018R\u03b1). Intraperitoneal injection of recombinant human IL\u201018\u2013binding protein, a specific inhibitor of IL\u201018, attenuated hyperoxic brain injury. Mice deficient in IL\u20101 receptor\u2013associated kinase 4 (IRAK\u20104), which is pivotal for both IL\u20101\u03b2 and IL\u201018 signal transduction, were protected against oxygen\u2010mediated neurotoxicity. These findings causally link IL\u20101\u03b2 and IL\u201018 to hyperoxia\u2010induced cell death in the immature brain. These cytokines might serve as useful targets for therapeutic approaches aimed at preserving neuronal function in the immature brain, which is exquisitely sensitive to a variety of iatrogenic measures including oxygen. 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