Human amnion epithelial cells modulate hyperoxia-induced neonatal lung injury in mice |
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| Authors: | Patricia Vosdoganes Rebecca Lim Eugenia Koulaeva Siow Teng Chan Rutu Acharya Timothy JM Moss Euan M Wallace |
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| Institution: | 1. The Ritchie Centre, Monash Institute of Medical Research, Clayton, Victoria, Australia;2. Department of Obstetrics and Gynecology, Monash University, Clayton, Victoria, Australia;1. Department of Medicine, University of Sherbrooke, Sherbrooke, Quebec;2. Department of Genetics, University of Sherbrooke, Sherbrooke, Quebec;3. Department of Medicine, University of Calgary, Calgary, Alberta, Canada;4. Division of Thoracic Surgery, University of Calgary, Calgary, Alberta, Canada;1. Department of Comparative Biomedical Sciences, University of Teramo, Teramo, Italy;2. Department of Biomorphology, University of Chieti, Chieti, Italy;3. Department of Biomedical Sciences, University of Chieti, Chieti, Italy;4. StemTech Group, Chieti, Italy;1. Department of Animal Science and Technology, National Taiwan University, Taipei, Taiwan;2. Institute of Biotechnology, National Taiwan University, Taipei, Taiwan |
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| Abstract: | Background aimsHuman amnion epithelial cells (hAECs) prevent pulmonary inflammation and injury in fetal sheep exposed to intrauterine lipopolysaccharide. We hypothesized that hAECs would similarly mitigate hyperoxia-induced neonatal lung injury.MethodsNewborn mouse pups were randomized to either normoxia (inspired O2 content (FiO2) = 0.21, n = 60) or hyperoxia (FiO2 = 0.85, n = 57). On postnatal days (PND) 5, 6 and 7, hAECs or sterile saline (control) was administered intraperitoneally. All animals were assessed at PND 14.ResultsHyperoxia was associated with lung inflammation, alveolar simplification and reduced postnatal growth. Administration of hAECs to hyperoxia-exposed mice normalized body weight and significantly attenuated some aspects of hyperoxia-induced lung injury (mean linear intercept and septal crest density) and inflammation (interleukin-1α, interleukin-6, transforming growth factor-β and platelet-derived growth factor-β). However, hAECs did not significantly alter changes to alveolar airspace volume, septal tissue volume, tissue-to-airspace ratio, collagen content or leukocyte infiltration induced by hyperoxia.ConclusionsIntraperitoneal administration of hAECs to neonatal mice partially reduced hyperoxia-induced lung inflammation and structural lung damage. These observations suggest that hAECs may be a potential therapy for neonatal lung disease. |
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