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Intrauterine growth restriction predisposes to airway inflammation without disruption of epithelial integrity in postnatal male mice.

Authors
  • Looi, Kevin1, 2
  • Kicic, Anthony1, 2, 3, 4, 5
  • Noble, Peter B6
  • Wang, Kimberley C W1, 6
  • 1 Telethon Kids Institute, The University of Western Australia, Crawley, WA6009, Australia. , (Australia)
  • 2 School of Public Health, Curtin University, Bentley, WA6102, Australia. , (Australia)
  • 3 Faculty of Health and Medical Science, The University of Western Australia, Crawley, WA6009, Australia. , (Australia)
  • 4 Department of Respiratory and Sleep Medicine, Perth Children's Hospital, Nedlands, WA6009, Australia. , (Australia)
  • 5 Centre for Cell Therapy and Regenerative Medicine, The University of Western Australia, Crawley, WA6009, Australia. , (Australia)
  • 6 School of Human Sciences, The University of Western Australia, Crawley, WA6009, Australia. , (Australia)
Type
Published Article
Journal
Journal of Developmental Origins of Health and Disease
Publisher
Cambridge University Press
Publication Date
Jun 01, 2021
Volume
12
Issue
3
Pages
496–504
Identifiers
DOI: 10.1017/S2040174420000744
PMID: 32799948
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Evidence from animal models demonstrate that intrauterine growth restriction (IUGR) alters airway structure and function which may affect susceptibility to disease. Airway inflammation and dysregulated epithelial barrier properties are features of asthma which have not been examined in the context of IUGR. This study used a maternal hypoxia-induced IUGR mouse model to assess lung-specific and systemic inflammation and airway epithelial tight junctions (TJs) protein expression. Pregnant BALB/c mice were housed under hypoxic conditions (10.5% O2) from gestational day (GD) 11 to 17.5 (IUGR group; term, GD 21). Following hypoxic exposure, mice were returned to a normoxic environment (21% O2). A Control group was housed under normoxic conditions throughout pregnancy. Offspring weights were recorded at 2 and 8 weeks of age and euthanized for bronchoalveolar lavage (BAL) and peritoneal cavity fluid collection for inflammatory cells counts. From a separate group of mice, right lungs were collected for Western blotting of TJs proteins. IUGR offspring had greater inflammatory cells in the BAL fluid but not in peritoneal fluid compared with Controls. At 8 weeks of age, interleukin (IL)-2, IL-13, and eotaxin concentrations were higher in male IUGR compared with male Control offspring but not in females. IUGR had no effect on TJs protein expression. Maternal hypoxia-induced IUGR increases inflammatory cells in the BAL fluid of IUGR offspring with no difference in TJs protein expression. Increased cytokine release, specific to the lungs of IUGR male offspring, indicates that both IUGR and sex can influence susceptibility to airway disease.

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