Umbilical cord stem cell therapy for bronchopulmonary dysplasia: ready for prime time?
- Department of Pediatrics, Pediatric Heart Lung Center, University of Colorado School of Medicine and Children's Hospital Colorado, Aurora, Colorado, USA
- Correspondence to Dr Christopher D Baker, Department of Pediatrics, Pediatric Heart Lung Center, University of Colorado School of Medicine, 13123 E. 16th Ave Box B-395, Aurora, CO 80045, USA;
- Received 18 December 2012
- Accepted 20 December 2012
- Published Online First 15 January 2013
Chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), emphysema, idiopathic pulmonary fibrosis, cystic fibrosis, pulmonary arterial hypertension and others contribute significantly to morbidity and mortality worldwide, yet successful interventions are often limited. Over the past decade, there has been an explosion of excitement regarding potential roles for stem cell therapies to prevent, repair or regenerate lung tissue to improve outcomes of these severe, progressive and often fatal disorders.1 ,2 Based on strong preclinical data, early clinical studies are currently underway to explore safety and potential efficacy in adults with chronic pulmonary diseases, including COPD, idiopathic pulmonary arterial hypertension and others.
In children, bronchopulmonary dysplasia (BPD) remains one of the more common yet challenging respiratory disorders for which current strategies are extremely limited. BPD is the chronic lung disease that develops in premature newborns who require respiratory support and oxygen therapy after birth.3–7 BPD has changed remarkably since its original description over 45 years ago, and remains a ‘moving target:’ a disease modulated and at least partly defined by the impact of therapeutic interventions themselves. Routine use of prenatal steroids, surfactant therapy, improved ventilator strategies and other treatments have improved survival and the clinical course of infants with BPD. Importantly, infants with BPD now have very different clinical courses, outcomes and pathology than had been traditionally observed in preterm infants during the presurfactant era. The classic progressive stages leading to marked disruption of lung architecture with prominent fibroproliferative disease and cyst-like lesions that characterised BPD in the past are now often absent, and the disease is now predominantly defined as a disruption of distal lung airspace and vascular growth.6–8 Lung histology of infants with the ‘new BPD’ often demonstrates far milder fibrosis and fewer signs of lung injury, but impaired alveolar and vascular growth remains prominent. …