Further, the increase in TUNEL-positive cells following ventilation, despite its significance, was not a substantial increase which is most likely due to the early time point at which apoptosis is being assessed. A limitation of our study is that although the effect of LPS on the brain has been well characterized, the effect of ventilation after IA LPS on brain inflammation and injury may be time dependent. We chose to assess the time of the peak fetal cytokine response to IA LPS; however, resultant alterations in the brain may not be apparent until later. Indeed, variability in timing of inflammation/infection and subsequent delivery is likely the cause of controversy surrounding the variable reports of associations between chorioamnionitis and neonatal morbidities including bronchopulmonary dysplasia, periventricular leukomalacia and intraventricular haemorrhage. A further limitation is that the duration of ventilation in our study may not have been sufficient to induce profound histological injury within the preterm brain. The duration of ventilation was chosen as it corresponds to the peak inflammatory cascade after ventilation onset. Indeed, increasing the duration of ventilation in preterm infants is known to increase the risk of WM injury. We compared our findings to unventilated preterm lambs to examine the influence of positive pressure ventilation versus a naı¨ve lung. It may be more appropriate to compare lung and brain inflammation and injury to spontaneously breathing lambs, but this is not possible at this gestation, as these lambs, even with antenatal corticosteroids, cannot maintain adequate respiratory support without significant intervention. Lastly, microglia were characterized as amoeboid if they had a large, densely stained soma with completely VE-821 protracted processes and all other Iba-1 positive cells were classified as ramified. This does not strictly differentiate between activated and resting microglia. Further analysis using TNF-a, CD68 and MHC I and MHC II would aid in phenotype differentiation which may have altered this interpretation, but this was beyond the scope of this study, and unlikely to impact significantly on our observed findings. In summary, ventilation after IA LPS resulted in a profound inflammatory response within the preterm ventilated lung and within the cerebral WM, with some histological indices of brain injury observed. However, a protective ventilation strategy was unable to reduce lung or brain inflammation and injury in preterm lambs after IA LPS. These studies indicate that the preterm infant exposed to chorioamnionitis likely has increased susceptibility to ventilation induced lung and brain injury. Cyanobacteria are ubiquitous in all arid and semi-arid biological soil crusts, where they play a vital role in fixing carbon and nitrogen, stabilizing the soil as well as altering the hydrological properties of crust-covered soils. The dominance of cyanobacteria in arid deserts is indicative of their eco-physiological adaptability to high temper.