Abstract
Exogenous surfactant is critical in the treatment of neonates with respiratory distress syndrome. Lucinactant (Surfaxin; Discovery Laboratories, Inc.) is a surfactant replacement therapy containing sinulpeptide, which may reduce lung inflammation. This study tested whether Lucinactant reduces markers of inflammation, damage and remodeling in human airway epithelial cells exposed to hyperoxia. Calu-3 monolayers cultured at an air–liquid interface were treated apically with 140 μL of normal saline, Lucinactant or Beractant (Survanta; Abbott Laboratories, Inc.). Treated monolayers were exposed to 60% O2/5% CO2 for 24 or 72 h. Transepithelial resistance (TER; p < 0.001) and cell viability (p < 0.05) were greater in both surfactant groups compared with saline; by 72 h Lucinactant cells had greater TER than Beractant (p < 0.001). Surfactant treated groups secreted less IL-8 than saline (p < 0.001), whereas Lucinactant cells secreted less IL-6 than saline and Beractant (p < 0.001). Matrix metalloproteinase 7, expressed by saline and Beractant treated cells at 24 h, was attenuated by 72 h by Beractant (p < 0.001), but was never detected in Lucinactant cells. Histology indicated less injury with Lucinactant relative to Beractant and saline. These data suggest that Lucinactant was protective compared with Beractant and control.
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Abbreviations
- ASF:
-
apical surface wash fluid
- BPD:
-
bronchopulmonary dysplasia
- KL4 (sinulpeptide):
-
synthetic peptide that mimics
- MMP:
-
matrix metalloproteinase SP-B
- SP-B:
-
surfactant protein B
- TER:
-
transepithelial resistance
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Acknowledgements
We thank Barbara E. Gray, B.A., CPM, Administrative Manager, Nemours Research Lung Center, for her contribution to the research effort.
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Supported by Discovery Laboratories, Inc. and NIH COBRE grant # 1P20 RR020173 (The Center for Pediatric Research).
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Zhu, Y., Miller, T., Chidekel, A. et al. KL4-Surfactant (Lucinactant) Protects Human Airway Epithelium from Hyperoxia. Pediatr Res 64, 154–158 (2008). https://doi.org/10.1203/PDR.0b013e318175dd14
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DOI: https://doi.org/10.1203/PDR.0b013e318175dd14
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