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Review
. 2022 Apr 9;11(8):1275.
doi: 10.3390/cells11081275.

Stem-Cell Therapy for Bronchopulmonary Dysplasia (BPD) in Newborns

Said A Omar  1   2 , Amal Abdul-Hafez  1 , Sherif Ibrahim  1 , Natasha Pillai  1 , Mohammed Abdulmageed  1   2 , Ranga Prasanth Thiruvenkataramani  1   2 , Tarek Mohamed  1   2 , Burra V Madhukar  1 , Bruce D Uhal  3
Affiliations
Review

Stem-Cell Therapy for Bronchopulmonary Dysplasia (BPD) in Newborns

Said A Omar et al. Cells. .

Abstract

Premature newborns are at a higher risk for the development of respiratory distress syndrome (RDS), acute lung injury (ALI) associated with lung inflammation, disruption of alveolar structure, impaired alveolar growth, lung fibrosis, impaired lung angiogenesis, and development of bronchopulmonary dysplasia (BPD) with severe long-term developmental adverse effects. The current therapy for BPD is limited to supportive care including high-oxygen therapy and pharmacotherapy. Recognizing more feasible treatment options to improve lung health and reduce complications associated with BPD is essential for improving the overall quality of life of premature infants. There is a reduction in the resident stem cells in lungs of premature infants with BPD, which strongly suggests a critical role of stem cells in BPD pathogenesis; this warrants the exploration of the potential therapeutic use of stem-cell therapy. Stem-cell-based therapies have shown promise for the treatment of many pathological conditions including acute lung injury and BPD. Mesenchymal stem cells (MSCs) and MSC-derived extracellular vesicles (EVs) including exosomes are promising and effective therapeutic modalities for the treatment of BPD. Treatment with MSCs and EVs may help to reduce lung inflammation, improve pulmonary architecture, attenuate pulmonary fibrosis, and increase the survival rate.

Keywords: bronchopulmonary dysplasia; extracellular vesicles; hyperoxia; lung injury; premature infants; stem cells.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic diagram illustration of the role of MSCs and secretion of their EVs in the treatment of hyperoxia-induced lung injury. As the preterm neonatal lung is exposed to excessive oxygen supplementation (hyperoxia) or infection (sepsis), proinflammatory cytokines are released, anti-inflammatory cytokines are inhibited, and oxidative stress occurs. These changes direct the conversion of M2 to M1 macrophage subsets, leading to structural lung damage/developmental abnormalities. MSCs are derived from various sources including bone marrow (BM), umbilical cord (UC), placenta, and adipose tissue. Treatment with MSCs or their secreted EVs alleviates the hyperoxia-induced lung injury through several mechanisms. These mechanisms include inhibition of proinflammatory cytokines and induction of anti-inflammatory cytokines, VEGF, and antioxidant pathways, leading to the transition of M1 to M2 macrophages, and the stimulation of differentiation of AT2 alveolar epithelial cells to AT1 alveolar epithelial cells. This illustration was created using BioRender.com.
See this image and copyright information in PMC

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