Intermittent neonatal hypoxia elicits the upregulation of inflammatory‐related genes in adult male rats through long‐lasting programming effects

The long‐term effects of neonatal intermittent hypoxia ( IH ), an accepted model of apnea‐induced hypoxia, are unclear. We have previously shown lasting “programming” effects on the HPA axis in adult rats exposed to neonatal IH . We hypothesized that neonatal rat exposure to IH will subsequently result in a heightened inflammatory state in the adult. Rat pups were exposed to normoxia (control) or six cycles of 5% IH or 10% IH over one hour daily from postnatal day 2–6. Plasma samples from blood obtained at 114 days of age were analyzed by assessing the capacity to induce transcription in a healthy peripheral blood mononuclear cell ( PBMC ) population and read using a high‐density microarray. The analysis of plasma from adult rats previously exposed to neonatal 5% IH versus 10% IH resulted in 2579 significantly regulated genes including increased expression of Cxcl1, Cxcl2, Ccl3, Il1a , and Il1b . We conclude that neonatal exposure to intermittent hypoxia elicits a long‐lasting programming effect in the adult resulting in an upregulation of inflammatory‐related genes.