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Updated: Jul 2, 2026
A Mouse Model of Intestinal Partial Obstruction
Published on: March 5, 2018
Epithelial changes of congenital intestinal obstruction in a rat model
Quentin Ballouhey1,2, Laurent Fourcade1,2, Laurence Richard1,3
1Myelin Maintenance and Peripheral Neuropathies, EA6309, University of Limoges, Limoges, France.
Insights
Congenital intestinal atresia in rat fetuses accelerated proximal segment maturation and disrupted the distal segment. Epithelial system (ES) gene expression changes suggest their involvement in this condition, beyond the enteric nervous system (ENS).
Area of Science:
- Developmental biology
- Gastroenterology
- Congenital disorders
Background:
- Intestinal atresia is a rare congenital condition often leading to severe bacterial infections post-surgery.
- Previous research primarily focused on the enteric nervous system (ENS) in intestinal atresia.
- This study investigates the potential role of epithelial systems (ES) in the pathophysiology of intestinal atresia.
Purpose of the Study:
- To explore the involvement of epithelial systems (ES) in the pathophysiology of congenital intestinal atresia.
- To analyze global gene expression patterns in a rat model of induced intestinal atresia, focusing on ES genes.
- To compare gene expression in proximal and distal segments of the fetal small intestine.
Main Methods:
- Transcriptomic analysis of global gene expression in rat fetal small intestines at various developmental stages.
- Focus on genes related to enterocytes and goblet cells (ES markers).
- Validation using histochemistry, electron microscopy, and RT-qPCR.
Main Results:
- Physiological increase in ES markers observed from ED15 to ED21 in control fetuses.
- Operated fetuses showed significantly higher gene expression variations in the proximal segment (absorption, epithelial barrier) compared to the distal segment.
- Increased goblet cells and markers were noted in the proximal segment of operated fetuses.
Conclusions:
- Fetal intestinal obstruction accelerates proximal segment maturation and disrupts the distal intestinal wall.
- Significant changes in epithelial cells suggest their involvement in intestinal disorders, extending beyond the ENS.
- Epithelial system alterations are implicated in the pathophysiology of congenital intestinal atresia.
Introduction:
Intestinal atresia is a rare congenital affliction that is often associated with severe bacterial infections despite adequate neonatal surgery. Previous studies have focused on enteric nervous system variations. We hypothesized that epithelial systems (ES) may also be involved in the pathophysiology of postnatal disorders.
Materials And Methods:
Global gene expression was measured by transcriptomic analysis in a rat model of induced intestinal atresia. The analyses then focused on genes involved in ES (enterocytes and goblet cells). Rat fetus small intestines at various stages of development (ED15, ED17, ED19, and ED21, n = 22), were used as non-operated controls and compared to the upper and lower segments of rat fetus small intestines with an induced atresia (n = 14; ligature at ED18). The pattern of gene expression was then confirmed by histochemistry, electron microscopy, and RT-qPCR.
Results:
From ED15 to ED21, the expression of several genes exhibited a physiological increase of ES markers, with a significant increase at the end of gestation. The operated embryos exhibited significantly higher variations of gene expression in the proximal segment than in the distal segment in terms of absorption and the epithelial barrier. An increase in goblet cells and markers was observed in the proximal segment compared to the controls.
Conclusion:
Fetal intestinal obstruction accelerates maturation in the proximal segment and disrupts the intestinal wall in the distal segment, with a decrease in the number of mucosal cells. Moreover, the epithelial cells underwent significant changes, supporting the notion that intestinal disorders involve more than the ENS.
Related Concept Videos
01:29Intestinal Obstruction I: Introduction
01:07Intestinal Obstruction II: Pathophysiology