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Updated: Apr 11, 2026
Modeling Ascending Vaginal Infection, Preterm Birth, and Neonatal Morbidity in Mice
Published on: October 10, 2025
The effect of prenatal maternal infection on respiratory function in mouse offspring: evidence for enhanced
Thilini D Samarasinghe1, Scott A Sands2, Elizabeth M Skuza1
1Ritchie Centre, MIMR-PHI Institute of Medical Research, Clayton, Victoria, Australia;
Insights
Maternal inflammation during pregnancy alters lung development and breathing control in offspring. These changes, including reduced lung function and increased respiratory sensitivity, persist long after birth.
Area of Science:
- Respiratory physiology
- Developmental biology
- Immunology
Background:
- Systemic maternal inflammation is linked to preterm birth and bronchopulmonary dysplasia.
- It may also cause long-term morbidities like reduced pulmonary function and cardiovascular issues.
Purpose of the Study:
- To investigate if antenatal maternal inflammation per se alters alveolar development and chemoreflex sensitivity in offspring.
- To determine if these changes persist beyond infancy.
Main Methods:
- Pregnant mice were exposed to lipopolysaccharide (LPS) or saline (SHAM) at embryonic day 16.
- Offspring lung structure and ventilatory responses to hypoxia, hypercapnia, and asphyxia were assessed at postnatal days 7, 28, and 60 using plethysmography.
Main Results:
- LPS-exposed pups exhibited reduced baseline ventilation and increased ventilatory responses to respiratory challenges, persisting until day 60.
- Alveolar septal thickness increased and alveolar number decreased in LPS pups, with effects diminishing by day 60.
- Increased apnea frequency was observed in LPS-exposed offspring.
Conclusions:
- Antenatal inflammation induces persistent deficits in lung structure and hypersensitive respiratory responses in offspring.
- These findings suggest antenatal inflammation contributes to impaired gas exchange and breathing instability in infants, potentially impacting long-term health.
Abstract:
Systemic maternal inflammation is implicated in preterm birth and bronchopulmonary dysplasia (BPD) and may induce morbidities including reduced pulmonary function, sleep-disordered breathing, and cardiovascular disorders. Here we test the hypothesis that antenatal maternal inflammation per se causes altered alveolar development and increased chemoreflex sensitivity that persists beyond infancy. Pregnant C57BL/6 mice were administered lipopolysaccharide (LPS) (150 μg/kg ip) to induce maternal inflammation or saline (SHAM) at embryonic day 16 (randomized). Pups were weighed daily. On days 7, 28, and 60 (D07, D28, and D60), unrestrained wholebody plethysmography quantified ventilation and chemoreflex responses to hypoxia (10%), hypercapnia (7%), and asphyxia (hypoxic hypercapnia). Lungs were harvested to quantify alveolar number, size, and septal thickness. LPS pups had reduced baseline ventilation per unit bodyweight (∼40%, P < 0.001) vs. SHAM. LPS increased ventilatory responses to hypoxia (D07: 66% vs. 28% increase in ventilation; P < 0.001) hypercapnia (170% vs. 88%; P < 0.001), and asphyxia (249% vs. 154%; P < 0.001); hypersensitive hypoxic responsiveness persisted until D60 (P < 0.001). LPS also increased apnea frequency (P < 0.01). LPS caused thicker alveolar septae (D07, P < 0.001), diminished alveolar number (D28, P < 0.001) vs. SHAM, but effects were minimal by D60. Pups delivered from mothers exposed to antenatal inflammation exhibit deficits in lung structure and hypersensitive responses to respiratory stimuli that persist beyond the newborn period. Antenatal inflammation may contribute to impaired gas exchange and unstable breathing in newborn infants and adversely affect long-term health.
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