Infections are important risk factors of perinatal brain injury. However, under certain circumstances, inflammation mediates preconditioning and provides protection to the immature brain. Recent experimental studies have examined the interaction of lipopolysaccharide (LPS) with other events. Evidence demonstrates that LPS administered 24h before hypoxia-ischemia in 7-day-old rats provides neuroprotection, which is associated with up-regulation of endogenous corticosterone but is also linked to significant cerebral gene regulation. Gene ontology analysis reveals that the most over-represented genes belong to immune and inflammatory processes. However, a number of cell death/survival genes, including complement component 1, complement component 3, aquaporin 4, epidermal growth factor receptor pathway substrate 15 and PYD and CARD domain containing are also significantly up-regulated 24h following LPS exposure. These results suggest that in addition to immune-related activation, transcription of cell death pathways may be important in LPS-induced preconditioning in the immature brain.