TY - JOUR
T1 - Inflammation-induced preterm lung maturation
T2 - Lessons from animal experimentation
AU - Moss, Timothy J M
AU - Westover, Alana
PY - 2017/6
Y1 - 2017/6
N2 - 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.
AB - 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.
KW - Bronchopulmonary dysplasia
KW - Glucocorticoids
KW - Inflammation
KW - Preterm
KW - Prostaglandins
KW - Respiratory distress syndrome
KW - Surfactant
UR - http://www.scopus.com/inward/record.url?scp=85006830468&partnerID=8YFLogxK
U2 - 10.1016/j.prrv.2016.10.004
DO - 10.1016/j.prrv.2016.10.004
M3 - Review Article
AN - SCOPUS:85006830468
VL - 23
SP - 72
EP - 77
JO - Paediatric Respiratory Reviews
JF - Paediatric Respiratory Reviews
SN - 1526-0542
ER -