Abstract
Bronchopulmonary dysplasia (BPD) remains a major complication of premature birth. Despite great achievements in perinatal medicine over the past decades, there is no treatment for BPD. Recent insights into the biology of stem/progenitor cells have ignited the hope of regenerating damaged organs. Animal experiments revealed promising lung protection/regeneration with stem/progenitor cells in experimental models of BPD and led to first clinical studies in infants. However, these therapies are still experimental and knowledge on the exact mechanisms of action of these cells is limited. Furthermore, heterogeneity of the therapeutic cell populations and missing potency assays currently limit our ability to predict a cell product’s efficacy. Here, we review the therapeutic potential of mesenchymal stromal, endothelial progenitor, and amniotic epithelial cells for BPD. Current knowledge on the mechanisms behind the beneficial effects of stem cells is briefly summarized. Finally, we discuss the obstacles constraining their transition from bench-to-bedside and present potential approaches to overcome them.
Highlights
The proper ventilation and oxygenation of a premature newborn is the foremost task in neonatology
This and other hostile extrauterine conditions leads to the chronic lung disease of prematurity or bronchopulmonary dysplasia (BPD)
There is no effective treatment for BPD and all present approaches remain either supportive, present major adverse effects or show only small benefits
Summary
The proper ventilation and oxygenation of a premature newborn is the foremost task in neonatology. Exogenous stem cells or their products derived from the mesenchymal [14,15,16,17,18,19,20,21,22,23,24,25,26], epithelial [27,28,29], or endothelial [30, 31] compartment of accessible tissue, such as the bone marrow, placenta, or the umbilical cord prevent or restore lung damage in animal models of BPD Most of these data have been generated in neonatal rodents exposed to hyperoxia, a model which will be discussed below. The function of specific lung-resident stem cells with mesenchymal, endothelial, and epithelial differentiation potential (lung side population cells) [60] is disrupted in murine hyperoxia-induced lung injury [61] These findings suggest that damage to endogenous MSCs may contribute to the disease pathogenesis of BPD. It is known that MSCs age during ex vivo expansion and that this influences biological properties of the TABLE 1 | MSCs in clinical trails for pulmonary diseases
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