| Fetal Alveolar Type II Cell Injury Induced by Short-term Exposure to Hyperoxia. |
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Hyeon Soo Lee |
1Department of Pediatrics, Kangwon National University Hospital, Kangwon National University School of Medicine, Chuncheon, Korea. premee@kangwon.ac.kr
2Institute of Medical Sciences, Kangwon National University School of Medicine, Chuncheon, Korea. |
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| Abstract |
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A High concentration of oxygen (>40%) is used as a life-saving therapy in preterm newborns since birth. By generating excess reactive oxygen species, however, hyperoxia can cause lung injury leading to bronchopulmonary dysplasia (BPD). Although hyperoxia-induced lung injury contributes to the evolution of BPD, the mechanisms by which hyperoxia contributes to the genesis of lung injury in preterm lungs are not yet fully defined, and there are no specific measures for the protection of preterm lungs against injury secondary to hyperoxia. Alveolar type II cells are key components of the alveolar structure, and they are responsible for the restoration of normal alveolar epithelium after acute lung injury. However, hyperoxia is primarily delivered to the alveolar epithelium and alveolar type II cells can be the main target for the injury secondary to hyperoxia. To date, my researches have been focused on injury of fetal alveolar type II cells exposed to hyperoxia and the role of anti-inflammatory cytokine, IL-10 minimizing fetal type II cell injury induced by hyperoxia.
Based on my previous studies, this article summarizes the cellular and molecular mechanisms of fetal type II cell injury induced in the early stage of hyperoxia and the protective potency of IL-10 in fetal alveolar type II cells and neonatal lungs injured by hyperoxia. |
| Key Words:
Hyperoxia; Fetal alveolar type II cells; IL-10 |
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