A study conducted by Kobe University has revealed that inflammation of the abdominal cavity in human fetuses, resulting from a perforation of their intestine, is likely caused by proteins found in their fetal stool. The condition, known as meconium peritonitis, is a life-threatening condition for babies with a mortality rate of 10%-15%. The researchers developed a new mouse model to replicate the condition in order to facilitate research and drug development for this challenging condition.
The researchers injected a slurry of meconium, taken from human newborns, into the abdominal cavities of mouse pups. They found that the mortality rate was not influenced by antibiotic treatment, indicating that the cause was not bacterial. However, when the meconium slurry was heat-treated to disrupt the natural shapes of proteins, they observed a significant reduction in mortality. This suggests that proteins in the meconium, particularly digestive enzymes, are responsible for causing inflammation in the abdominal cavity.
The team further characterized the condition of the mice pups by analyzing their biochemical and gene expression profiles. By comparing their results to a previously established mouse model, where pups were injected with an extract of intestinal contents from adult mice, they determined that their model resulted in different symptoms. They believe that their model is specific to meconium-caused inflammation and can serve as a valuable platform for conducting further research on the condition.
The researchers hope that their work will lead to the development of effective treatments for meconium peritonitis, which affects about one in every 35,000 live births. They emphasize the simplicity and reproducibility of their mouse model, enabling researchers to elucidate the pathophysiology of the condition. This research was funded by various organizations, including the Japan Society for the Promotion of Science and the Japan Foundation for Pediatric Research.
Overall, the study conducted by Kobe University sheds light on the role of proteins in fetal stool in causing inflammation of the abdominal cavity in human fetuses. By developing a new mouse model to replicate the condition, the researchers have provided a valuable tool for further research and drug development for meconium peritonitis. Their findings suggest that proteins, particularly digestive enzymes, are likely responsible for the inflammation, and they hope that their work will lead to the development of effective treatments for this life-threatening condition that affects a small percentage of newborns.