title: Human amnion epithelial cells modulate hyperoxia-induced neonatal lung injury in mice.
abstract: OBJECTIVE
  Human 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.
  
  
  METHODS
  Newborn 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.
  
  
  RESULTS
  Hyperoxia 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.
  
  
  CONCLUSIONS
  Intraperitoneal 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.
authors: The Ritchie Centre, Monash Institute of Medical Research, Clayton, Victoria, Australia.
authors: Patricia
authors: P
authors: Vosdoganes
authors: Rebecca
authors: R
authors: Lim
authors: Eugenia
authors: E
authors: Koulaeva
authors: Siow Teng
authors: ST
authors: Chan
authors: Rutu
authors: R
authors: Acharya
authors: Timothy J M
authors: TJ
authors: Moss
authors: Euan M
authors: EM
authors: Wallace
mesh_terms: D000650:Amnion / Q000166:cytology*; D000818:Animals; D002478:Cells, Cultured; D004847:Epithelial Cells / Q000166:cytology* / Q000637:transplantation*; D005260:Female; D006801:Humans; D006931:Hyperbaric Oxygenation; D018496:Hyperoxia / Q000150:complications*; D007231:Infant, Newborn; D053582:Interleukin-1alpha / Q000235:genetics; D015850:Interleukin-6 / Q000235:genetics; D055370:Lung Injury / Q000209:etiology* / Q000628:therapy*; D051379:Mice; D008810:Mice, Inbred C57BL; D010982:Platelet-Derived Growth Factor / Q000235:genetics; D011247:Pregnancy; D012333:RNA, Messenger / Q000096:biosynthesis; D016212:Transforming Growth Factor beta / Q000235:genetics
chemical_list: D053582:Interleukin-1alpha; D015850:Interleukin-6; D010982:Platelet-Derived Growth Factor; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta
keywords: bronchopulmonary dysplasia; chronic lung disease; human amnion epithelial cells; hyperoxia; neonatal lung disease