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A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
Inflammatory response in a rat model of gastroschisis is associated with an increase of NF-kappaB
L Sbragia1, A F Schmidt, S Moraes
1Disciplina de Cirurgia Pediátrica, Departamento de Cirurgia, Universidade Estadual de Campinas, SP, Brasil. sbragia@fmrp.usp.br
Insights
Gastroschisis in rat models causes intestinal injury and inflammation. This study found increased NF-kappaB in the intestine and liver of affected fetuses, indicating a key inflammatory marker.
Area of Science:
- Developmental biology
- Gastroenterology
- Immunology
Background:
- Gastroschisis is a congenital defect with high infant morbidity.
- Inflammatory bowel injury in gastroschisis is linked to amniotic fluid exposure.
- Understanding the inflammatory response is crucial for improving outcomes.
Purpose of the Study:
- To investigate inflammatory response components in the intestine and liver of a rat model of gastroschisis.
- To identify specific inflammatory markers associated with gastroschisis-induced injury.
Main Methods:
- A surgical rat model of gastroschisis was established at 18.5 days of gestation.
- Fetuses were grouped into gastroschisis, control, and sham.
- Measurements included organ weights, intestine length, and levels of cytokines (IL-1beta, IL-6, IL-10, TNF-alpha, IFN-gamma) and NF-kappaB via ELISA.
Main Results:
- Gastroschisis fetuses exhibited reduced intestine length and increased intestine weight.
- Intestine length correlated with liver weight in gastroschisis fetuses.
- NF-kappaB levels were significantly elevated in both the intestine and liver of gastroschisis fetuses.
Conclusions:
- The rat model effectively mimics key features of human gastroschisis.
- Elevated NF-kappaB in the intestine and liver signifies a critical inflammatory pathway in gastroschisis.
- Further research into NF-kappaB modulation may offer therapeutic targets.
Abstract:
Babies with gastroschisis have high morbidity, which is associated with inflammatory bowel injury caused by exposure to amniotic fluid. The objective of this study was to identify components of the inflammatory response in the intestine and liver in an experimental model of gastroschisis in rats. The model was surgically created at 18.5 days of gestation. The fetuses were exposed through a hysterotomy and an incision at the right of the umbilicus was made, exposing the fetal bowel. Then, the fetus was placed back into the uterus until term. The bowel in this model had macro- and microscopic characteristics similar to those observed in gastroschisis. The study was conducted on three groups of 20 fetuses each: gastroschisis, control, and sham fetuses. Fetal body, intestine and liver weights and intestine length were measured. IL-1beta, IL-6, IL-10, TNF-alpha, IFN-gamma and NF-kappaB levels were assessed by ELISA. Data were analyzed statistically by ANOVA followed by the Tukey post-test. Gastroschisis fetuses had a decreased intestine length (means +/- SD, 125 +/- 25 vs 216 +/- 13.9; P < 0.005) and increased intestine weight (0.29 +/- 0.05 vs 0.24 +/- 0.04; P < 0.005). Intestine length correlated with liver weight only in gastroschisis fetuses (Pearson's correlation coefficient, r = 0.518, P = 0.019). There were no significant differences in the concentrations of IL-1beta, TNF-alpha or IFN-gamma in the intestine, whereas the concentration of NF-kappaB was increased in both the intestine and liver of fetuses with gastroschisis. These results show that the inflammatory response in the liver and intestine of the rat model of gastroschisis is accompanied by an increase in the amount of NF-kappaB in the intestine and liver.
