Abstract
Children born preterm often exhibit reduced lung function and increased severity of response to respiratory viruses, suggesting that premature birth has compromised proper development of the respiratory epithelium and innate immune defenses. Increasing evidence suggests that premature birth promotes aberrant lung development likely due to the neonatal oxygen transition occurring before pulmonary development has matured. Given that preterm infants are born at a point of time where their immune system is also still developing, early life oxygen exposure may also be disrupting proper development of innate immunity. Here, we review current literature in hopes of stimulating research that enhances understanding of how the oxygen environment at birth influences lung development and host defense. This knowledge may help identify those children at risk for disease and ideally culminate in the development of novel therapies that improve their health.
Highlights
Growing evidence suggest gene–environment interactions during critical stages of development profoundly influence health later in life
Widespread methylation was detected in the blood of extremely preterm infants, suggesting that there were changes in blood cell development, composition, and perhaps immune function [27]. Since these changes in methylation resolved by 18 years of age, they may not be responsible for the long-term health effects reported in people born preterm
During recovery from naphthalene depletion, a population of Club cells proliferates from neuroendocrine bodies and from the bronchoalveolar duct junction (BADJ) [51, 52]. These bronchoalveolar stem cells (BASC) express airway Scgb1a1, alveolar Type II surfactant protein (SP)-C, the stem cell markers Sca-1, and CD34, but not CD45 [53]. These BASCs are able to self-renew and maintain expression of both airway Scgb1a1and alveolar SP-C expression when cultured on irradiated mouse embryonic fibroblasts
Summary
Growing evidence suggest gene–environment interactions during critical stages of development profoundly influence health later in life. Children born preterm often display reduced lung function, increased re-hospitalization following a respiratory viral infection, and incidence of non-atopic asthma [20, 21] They may show neurodevelopmental delay and have greater risk for high blood pressure and heart disease as adults [22, 23]. Widespread methylation was detected in the blood of extremely preterm infants, suggesting that there were changes in blood cell development, composition, and perhaps immune function [27] Since these changes in methylation resolved by 18 years of age, they may not be responsible for the long-term health effects reported in people born preterm. Because the pathogenesis of neonatal oxygen exposure in humans and in animal models has been recently reviewed [19, 35,36,37,38,39,40], the following discusses oxygen-induced changes in lung development in relationship to how it perturbs host response to respiratory viral infections
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