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.
Highlights
Gastroschisis affects 1.62/10,000 liveborns [1] and this incidence is increasing worldwide [2]
The survival rate of neonates with gastroschisis has increased in the last decades
Intestinal damage is still responsible for the increased morbidity and eventual mortality of these patients
Summary
Gastroschisis affects 1.62/10,000 liveborns [1] and this incidence is increasing worldwide [2]. The intestine presents loss of contractility, decreased enzymatic activity of the villi and alterations in collagen synthesis in the submucosal region [5]. These histological [6,7] and biochemical [8,9] abnormalities resulting from inflammation have been demonstrated in both experimental models and humans. Among the proinflammatory cytokines involved in intestinal lesions are tumor necrosis factor-α (TNF-α), IL-6 and interferon-gamma (IFN-γ) [11] All of these factors may be stimulated by the activation of hepatic NF-kappa. When the cells are stimulated, NF-kappaB is released and migrates to the nucleus, where it interacts with a specific sequence in the region that promotes target genes [12]
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