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KMID : 1034820220180010047
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Molecular & Cellular Toxicology
2022 Volume.18 No. 1 p.47 ~ p.56
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Core fucosylation of maternal milk N-glycan prevents intestinal inflammation by regulating Treg/Th17 balance in infant gut microbiota
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Tao Jia
Ran Yan
Pan Zhongmin
Wang Li
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Abstract
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Background: This study elucidated the regulatory roles of milk glycoprotein core fucosylation on the gut microbiota of breast-fed infants.
Objectives: In order to investigate the effects of core fucosylation of maternal milk N-glycan on the intestinal functions in newborn mice, Fut8+/+?→?Fut8+/+ and Fut8±?→?Fut8+/+ models were established.
Results: The results indicated that the gut microbiota diversity was altered and production of Bifidobacterium and Lactobacillus was reduced in the intestine of Fut8±?→?Fut8+/+mice. Furthermore, the levels of SCFAs were decreased in the gut of Fut8±?→?Fut8+/+infant. To further investigate the effects of core fucosylation of breast milk N-glycan on the intestinal inflammation in newborns, NEC models were established, and Fut8+/+ off-springs with experimentally induced NEC were fed with the breast milk of Fut8+/+ and Fut8± maternal mice. Our data revealed that reduced core fucosylation of breast milk N-glycan could be responsible for the intestinal inflammation in NEC offspring, as the production of pro-inflammatory cytokines including IL-1b, IL-6, IL-17A and TNF-a was significantly upregulated in Fut8±?→?Fut8+/+NEC group, while the levels of anti-inflammatory cytokine IL-10 were remarkably reduced. Furthermore, Treg/Th17 balance in the intestine was disturbed in Fut8±?→?Fut8+/+NEC newborn, suggesting the impaired immune development caused by reduced core fucosylation of breast milk.
Conclusion: These findings indicated that core fucosylation of maternal milk N-glycan could assist the colonization of gut Lactobacillus and Bifidobacterium and regulate the Treg/Th17 balance, subsequently preventing intestinal inflammation in breast-fed newborns.
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KEYWORD
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Fuscosylation, Maternal milk, N-glycan, Intestinal inflammation, Treg/Th17
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