Limits...
Affect of Early Life Oxygen Exposure on Proper Lung Development and Response to Respiratory Viral Infections.

Domm W, Misra RS, O'Reilly MA - Front Med (Lausanne) (2015)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, School of Medicine and Dentistry, The University of Rochester , Rochester, NY , USA ; Department of Environmental Medicine, School of Medicine and Dentistry, The University of Rochester , Rochester, NY , USA.

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.

No MeSH data available.


Related in: MedlinePlus

The early life oxygen environment affects changes in genetic as well as innate immune mechanisms. Cartoon depicting the affect early life oxygen environment imparts on genes that specify lung structure and function with cells involved in innate immunity.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4530667&req=5

Figure 2: The early life oxygen environment affects changes in genetic as well as innate immune mechanisms. Cartoon depicting the affect early life oxygen environment imparts on genes that specify lung structure and function with cells involved in innate immunity.

Mentions: As discussed previously, the transition to an oxygen environment at birth may be one of the most profound environmental changes one will ever experience and can lead to disease when it occurs inappropriately. Lungs of infants born preterm are often in the saccular phase of development. Alveolar regions at this time have yet to develop into true gas-exchanging structures, which is why many preterm infants develop respiratory distress. Furthermore, the capillary network surrounding the alveolus, which shuttles oxygen to the circulation, has yet to effectively complement the alveolus (96). Despite the life-saving efficacy of supplemental oxygen treatment during this critical time, growing evidence suggests that this treatment contributes to bronchopulmonary dysplasia (BPD), a chronic lung disease that is characterized by alveolar simplification and restrictive airways (16, 30). Oxygen-dependent changes in genes specifying lung structure and cell phenotype are likely to impact cells and molecules involved in innate immunity required for a proper host response to respiratory viral infection (Figure 2). This includes alveolar epithelial type II cells, goblet cells, eosinophils, macrophages, dendritic cells, T cells, B cells, and innate lymphoid cells, in addition to soluble mediators produced by these cells, including SPs, cytokines, chemokines, and mucus proteins mediate innate immunity (97–100). In other words, early life oxygen exposure or other oxidative stresses may drive the development of long-term lung disease by disrupting a delicate balance of cell communication between genes controlling lung development and innate immunity.


Affect of Early Life Oxygen Exposure on Proper Lung Development and Response to Respiratory Viral Infections.

Domm W, Misra RS, O'Reilly MA - Front Med (Lausanne) (2015)

The early life oxygen environment affects changes in genetic as well as innate immune mechanisms. Cartoon depicting the affect early life oxygen environment imparts on genes that specify lung structure and function with cells involved in innate immunity.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4530667&req=5

Figure 2: The early life oxygen environment affects changes in genetic as well as innate immune mechanisms. Cartoon depicting the affect early life oxygen environment imparts on genes that specify lung structure and function with cells involved in innate immunity.
Mentions: As discussed previously, the transition to an oxygen environment at birth may be one of the most profound environmental changes one will ever experience and can lead to disease when it occurs inappropriately. Lungs of infants born preterm are often in the saccular phase of development. Alveolar regions at this time have yet to develop into true gas-exchanging structures, which is why many preterm infants develop respiratory distress. Furthermore, the capillary network surrounding the alveolus, which shuttles oxygen to the circulation, has yet to effectively complement the alveolus (96). Despite the life-saving efficacy of supplemental oxygen treatment during this critical time, growing evidence suggests that this treatment contributes to bronchopulmonary dysplasia (BPD), a chronic lung disease that is characterized by alveolar simplification and restrictive airways (16, 30). Oxygen-dependent changes in genes specifying lung structure and cell phenotype are likely to impact cells and molecules involved in innate immunity required for a proper host response to respiratory viral infection (Figure 2). This includes alveolar epithelial type II cells, goblet cells, eosinophils, macrophages, dendritic cells, T cells, B cells, and innate lymphoid cells, in addition to soluble mediators produced by these cells, including SPs, cytokines, chemokines, and mucus proteins mediate innate immunity (97–100). In other words, early life oxygen exposure or other oxidative stresses may drive the development of long-term lung disease by disrupting a delicate balance of cell communication between genes controlling lung development and innate immunity.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, School of Medicine and Dentistry, The University of Rochester , Rochester, NY , USA ; Department of Environmental Medicine, School of Medicine and Dentistry, The University of Rochester , Rochester, NY , USA.

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.

No MeSH data available.


Related in: MedlinePlus