The Relationship Between Fucosylation Of Intestinal Epithelial Cells And Neonatal Necrotizing Enterocolitis

Objective: To probe the change of fucosylation of intestinal epithelial cells in NEC mouse model and discuss the possible mechanism.Methods: Forty-two 10-day old C57BL/6 mice were divided into NEC group(n=21,NEC model was established by artificial feeding,hypoxia and cold stimulation)and control group(n=21,feeded by the mother and no other treatment)by random number table,and newborn mice were sacrificed 3 days after modeling.The NEC pathological injury score was used to evaluate the effect of NEC modeling.The ratios of fucosylated intestinal epithelial cells(F-ECs)and intestinal lamina propria 3 type innate lymphocytes(ILC3s)were detected by flow cytometry.Interleukin-22(IL-22)of lamina propria lymphocyte and interleukin-22 receptor(IL-22R),fucosyltransferase 2(Fut2)of intestinal epithelial cells were tested by real-time quantitative PCR.Enzyme-linked immunosorbent assay(ELISA)was used to detect the level of IL-22 protein in lamina propria.Results: we successfully established the NEC mouse model.The results of flow cytometry showed that the percentage of F-ECs in the NEC model group was lower than that in the control group(28.41%±8.28% vs.43.60%±13.58%,P<0.05).The percentage of intestinal ILC3 s in the NEC model group was also significantly lower than that in the control group(11.59%±2.25% vs.20.14%±4.27%)and the difference was statistically significant(P<0.001).The results of real-time quantitative PCR showed that the mRNA levels of IL-22 R and Fut2 in epithelial cells of NEC model group were significantly lower than those in the control group(P<0.001).The mRNA level of IL-22 in lamina propria lymphocytes of NEC model group was also significantly lower than that in the control group(P<0.01).The expression level of IL-22 protein in lamina propria lymphocytes was lower in the NEC model group than that in the control group(P<0.001).Conclusions: Decreased fucosylation of intestinal epithelial cells is involved in the pathogenesis of NEC mouse model,and the mechanism may be related to the ILC3s-IL-22-Fut2 axis.