Preterm infant immaturity is characterised by unstable respiratory control, with male infants exhibiting particular vulnerability. Animal models of oxygen fluctuations during early life, have been previously demonstrated to cause persistent alterations in the control of breathing. Very preterm infants are at an increased risk of early life infection as a result of their immaturity and prolonged hospital stays. Late onset infection is a major challenge in very preterm infants. Proteins from Gram-positive bacteria such as (Lipoteichoic Acid) and PGN (Peptidoglycan) are known to mediate systemic inflammation through activation of multiple receptors, such as Toll-like receptors. We hypothesised that chronic exposure to intermittent hypoxia and hyperoxia (cIHH) prior to a subsequent Gram-positive bacterial infection would cause cardiorespiratory dysregulation. This study was conducted in line with European regulations and approved by local animal ethics committee at University College Cork and the national regulatory body, HPRA Ireland. Sprague Dawley rat litters (male and female pups) were exposed for 10 consecutive days to either Sham or cIHH treatment from postnatal day (PND) 3 to PND 12. On PND 13 blood samples were taken by cardiac puncture, one hour after i.p. administration of LTA&PGN. The steroid hormones oestradiol, progesterone and testosterone were measured in plasma. All data were analysed using a 3-way ANOVA (factors: sex, gas, drug). In a separate cohort in vivo respiratory function was assessed by whole body plethysmography. Assessment of sex steroids revealed that oestradiol concentrations were not changed by cIHH or LTA&PGN treatment. There was a higher concentration of testosterone in male pups compared to female pups (sex factor P<0.05), which was suppressed in cIHH treated animals (Gas factor P<0.05) but the interaction (sex x gas) was not statistically significant. Progesterone was enhanced by LTA&PGN treatment (P<0.05), this effect was most evident in males (sex x drug interaction P<0.05) but independent of gas treatment. We have revealed increased progesterone concentrations during infection in our animal model of early life stress. Although progesterone is a known respiratory stimulant, we have previously reported during normoxia, a decrease in both minute ventilation and CO2 production in response to LTA&PGN such that the ventilatory equivalent, in both male and female pups, was normal in this animal model. We will examine the hypoxic and asphyxic ventilatory response in a follow-up study to determine if the drug induced progesterone is a protective homeostatic mechanism. Further research is needed to identify the physiological basis for both vulnerability and resilience to infection during early life.