One study did examine nasal AEC cultured from 15 infants. However, the youngest infant was a month old, they were ‘held tightly by a nurse’ and because they were sedated with paracetamol and rectal midazolam they had to be monitored for 8 hours. This study also reported a single episode of epistaxis in their 15 subjects. In contrast, we observed no epistaxis in 155 neonates, this being most AbMole Aristolochic-acid-A likely due to the smaller diameter of our sampling brush, compared with the 5.5 mm brush used in the previous study. The paucity of erythrocytes identified in the cytospin preparations would suggest that the sampling procedure is relatively atraumatic in our hands. Our AbMole Niflumic acid methodology for sampling nasal AEC by nasal brushing in non-sedated neonates could prove a useful research tool and is especially applicable to large longitudinal studies. In addition to investigating the effect of in-utero influences on AEC phenotype, procuring neonatal airway epithelial tissue for culture has a variety of potential applications. As well as functional studies in submerged monolayers, it is likely that that our method could be adapted to grow neonatal nasal AEC in air-liquid interface cultures, which are thought to be more representative of conditions in vivo, this work is underway. Furthermore, obtaining nasal airway epithelial cells shortly after birth represents a privileged source of “na? ��ve” tissue not yet exposed to the modifying effects of post natal environmental pollutants and pathogens. As such, the tissue specific epigenetic effects of such exposures throughout life on the expression of 
genes involved in inflammatory mediator release could be explored. Based on our previous success culturing nasal airway epithelial cells from both adults and children, a study investigating repeated isolation of nasal cells from the same individual over time would be feasible. If neonatal nasal AEC are shown to be associated with subsequent asthma/allergic rhinitis and recognized/putative risk factors for these conditions, it may be possible to use neonatal nasal AEC as a neonatal biomarker in antenatal intervention studies. In the clinical setting it may be possible to use neonatal nasal AEC as a predictive biomarker to quantify subsequent risk of asthma. Of particular importance will be to confirm the hypothesis that the AEC of neonates who subsequently develop childhood asthma differ from AEC of children who do not develop asthma. In addition it will be important to ascertain whether neonatal AEC function is associated with established risk factors for childhood asthma, e.g. parental asthma, maternal smoking and maternal diet. Indeed we are currently using the methodology developed and reported here in an ongoing birth cohort study that is aimed at addressing some of these issues.