Abstract
Bronchopulmonary dysplasia (BPD) is the chronic lung disease of prematurity that affects very preterm infants. Although advances in perinatal care have changed the course of lung injury and enabled the survival of infants born as early as 23-24 weeks of gestation, BPD still remains a common complication of extreme prematurity, and there is no specific treatment for it. Furthermore, children, adolescents, and adults who were born very preterm and developed BPD have an increased risk of persistent lung dysfunction, including early-onset emphysema. Therefore, it is possible that early-life pulmonary insults, such as extreme prematurity and BPD, may increase the risk of COPD later in life, especially if exposed to secondary challenges such as respiratory infections and/or smoking. Recent advances in our understanding of stem/progenitor cells and their potential to repair damaged organs offer the possibility of cell-based treatments for neonatal and adult lung injuries. This paper summarizes the long-term pulmonary outcomes of preterm birth and BPD and discusses the recent advances of cell-based therapies for lung diseases, with a particular focus on BPD and COPD.
Highlights
Intrauterine and early postnatal environments have been shown to play an in uential role in the development and maturation of the lung [1]
Wong and colleagues [2] showed that survivors of moderate-severe bronchopulmonary dysplasia (BPD) presented with emphysema in early adulthood (17–33 years of age)
Many fetal and postnatal factors associated with preterm birth modulate the pathogenesis of BPD, including severity or prematurity, oxidative stress from supplemental oxygen therapy, ventilator-induced lung injury, fetal and/or postnatal infection or in ammation, and nutrition [6, 7]; identi cation of the injurious factors contributing to the development of BPD is o en hampered by its multifactorial etiology
Summary
Intrauterine and early postnatal environments have been shown to play an in uential role in the development and maturation of the lung [1]. Suboptimal conditions that interfere with normal development may result in altered lung structure and function and increase the risk for disease later in life. The onset of adult lung disease following inadequate development and maturation is becoming apparent at an early age. Wong and colleagues [2] showed that survivors of moderate-severe bronchopulmonary dysplasia (BPD) presented with emphysema in early adulthood (17–33 years of age). Understanding how the fetus and developing lung responds to intrauterine alterations and adapts to the postnatal environment can teach us about basic biology and the implications for adult lung diseases [3, 4]
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