Prenatal Melatonin Therapy Enhances Postnatal Lung Development in a Mouse Model of Inflammation-Induced Preterm Birth

Area of Science:

• Reproductive Biology
• Neonatal Development
• Pulmonary Medicine

Background:

• Inflammation-induced preterm birth (IPTB) severely impacts neonatal lung development, leading to impaired pulmonary function.
• Current treatments for lung maturation in preterm infants lack efficacy and safety.
• Melatonin's anti-inflammatory and antioxidant properties suggest potential benefits, but its effects on fetal lung maturation are not well understood.

Purpose of the Study:

• To evaluate the therapeutic efficacy of melatonin in preventing IPTB and improving fetal lung maturation in a mouse model.
• To investigate melatonin's impact on inflammatory markers, placental function, and lung development in IPTB.

Main Methods:

• A mouse model of intrauterine inflammation-induced preterm birth (IPTB) using lipopolysaccharide (LPS) was established.
• Pregnant mice at gestational day 17 received LPS, with or without melatonin treatment.
• Uterine and fetal lung tissues were analyzed for molecular and histological changes at various time points.

Main Results:

• Melatonin significantly reduced the rate of preterm birth induced by LPS.
• Melatonin downregulated pro-inflammatory genes, restored placental blood flow, and increased lamellar body counts in fetal lungs.
• Melatonin treatment improved fetal lung structure, enhanced surfactant protein B expression, and promoted lung development in surviving offspring.

Conclusions:

• Melatonin effectively prevents inflammation-induced preterm birth in a mouse model.
• Melatonin mitigates uterine inflammation and supports fetal lung maturation, improving pulmonary outcomes.
• Melatonin demonstrates significant therapeutic potential for managing IPTB and enhancing neonatal lung health.