Inflammation of the abdominal cavity in human fetuses resulting from a perforation of their intestine is likely to be caused by proteins contained in the fetal stool. This is the result of a Kobe University study that established a new mouse model allowing research and drug development for a condition that is otherwise difficult to approach. The fetus's stool, called the "meconium," is sterile but nevertheless causes inflammation of the abdominal cavity when it leaks out of the intestine after a perforation.
Called "meconium peritonitis," this is a life-threatening condition for the baby with a mortality rate of 10–15% in humans, and neither a cause nor a treatment have been established. The Kobe University pediatrician Fujioka Kazumichi and his team therefore decided to replicate the condition in mice. Since the intestinal development of mice and humans is different, the intestine of a newborn mouse pup is equivalent to that of a human fetus after the 12th week of pregnancy, but even so, the mouse pup is too small and fragile to induce the condition through an operation.
The research team therefore created a slurry of meconium, which they took from human newborns, and injected it into the abdominal cavity of the pups. They then characterized the resulting condition and compared the pups' mortality rates in response to different treatments. Their results, published in the journal Pediatric Research , show that mortality was not influenced by antibiotic treatment, ruling out.