Inflammatory response in a rat model of gastroschisis is associated with an increase of NF-kappaB.

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.