A Kobe University study found that proteins in fetal stool likely cause abdominal inflammation in human fetuses when the intestine is perforated. This condition, known as “meconium peritonitis,” is life-threatening, with a 10%-15% mortality rate. The study introduced a new mouse model to aid research and drug development for this difficult-to-treat condition.
Dr. Fujioka Kazumichi and his Kobe University team replicated a fetal condition in mice by injecting a meconium slurry from human newborns into the pups’ abdomens. Their study found that antibiotic treatment didn’t affect mortality, ruling out bacteria as the cause.
However, heat-treating the meconium, which disrupts proteins, significantly reduced mortality. This suggests that proteins, especially digestive enzymes in the meconium, cause inflammation.
The Kobe University team found that their mouse model, which uses a meconium slurry, causes symptoms different from those of a model using adult mouse intestinal contents. This suggests their model is specific to meconium-caused inflammation.
Researchers believe it will help research and find a treatment for meconium peritonitis, which affects 1 in 35,000 births. The team emphasizes that their model is simple and reliable for studying the disease.
The study concludes that proteins in fetal stool, specifically digestive enzymes, are likely responsible for causing abdominal inflammation in fetuses. This new mouse model can help researchers better understand and develop treatments for the condition.
Journal reference :
- M. Ashina et al, A neonatal mouse model of meconium peritonitis generated using human meconium slurry. Pediatric Research. DOI: 10.1038/s41390-024-03470-3.