Inflammation-induced preterm lung maturation: Lessons from animal experimentation

Timothy J M Moss, Alana Westover

Research output: Contribution to journalReview ArticleOtherpeer-review

7 Citations (Scopus)

Abstract

Intrauterine inflammation, or chorioamnionitis, is a major contributor to preterm birth. Prematurity . per se is associated with considerable morbidity and mortality resulting from lung immaturity but exposure to chorioamnionitis reduces the risk of neonatal respiratory distress syndrome (RDS) in preterm infants. Animal experiments have identified that an increase in pulmonary surfactant production by the preterm lungs likely underlies this decreased risk of RDS in infants exposed to chorioamnionitis. Further animal experimentation has shown that infectious or inflammatory agents in amniotic fluid exert their effects on lung development by direct effects within the developing respiratory tract, and probably not by systemic pathways. Differences in the effects of intrauterine inflammation and glucocorticoids demonstrate that canonical glucocorticoid-mediated lung maturation is not responsible for inflammation-induced changes in lung development. Animal experimentation is identifying alternative lung maturational pathways, and transgenic animals and cell culture techniques will allow identification of novel mechanisms of lung maturation that may lead to new treatments for the prevention of RDS.

Original languageEnglish
Pages (from-to)72-77
Number of pages6
JournalPaediatric Respiratory Reviews
Volume23
DOIs
Publication statusPublished - Jun 2017

Keywords

  • Bronchopulmonary dysplasia
  • Glucocorticoids
  • Inflammation
  • Preterm
  • Prostaglandins
  • Respiratory distress syndrome
  • Surfactant

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