333 Increased Expression of Anti-Inflammatory IL10 and IL10 Receptor in the Newborn Rat Brain Caused by Hyperoxia

Background: In neonatal medicine, oxygen is frequently used in the treatment of respiratory diseases, and preterm infants are generally exposed to relative hyperoxia compared to in-utero conditions. Recently, oxygen has been identified to cause apoptosis in the brain of newborn rats and rodents. Therefore, it may contribute to the development of cerebral palsy and neurocognitive defects often seen in preterm infants. Pro-inflammatory cytokines, i.e. IL-1b and IL-18, have been proven to be involved in neuronal apoptosis caused by hyperoxia. In contrast, IL-10 is an anti-inflammatory and anti-apoptotic cytokine that may have neuro-protective properties.Methods: We analysed expression of IL-10 receptor (IL-10R) and IL-10 in cortex and thalamus of six day old newborn Wistar rats (P6) exposed to 80% oxygen for 0, 2, 6, 12, 24 and 48 hours. mRNA levels were determined by semiquantitative reverse transcription polymerase chain reaction, and protein expression was analysed by immunoblotting.Results: Compared to rats not exposed to hyperoxia, mRNA of IL-10 and IL-10R increased markedly during oxygen exposure with peak levels at 6 and 24 hours, respectively (IL-10R: p<0.01, IL-10: p=0.01). A four-fold upregulation of IL-10R protein was found at 24 hours.Conclusions: Expression of anti-inflammatory IL-10 and IL-10R in the brain of newborn rats is upregulated during exposure to neurotoxic doses of oxygen. IL-10 may act as an internal neuroprotective agent against hyperoxia-induced cell death.