D-serine alleviates colitis by regulating intestinal α1,2-fucosylation

IF 4.8 1区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY
Ye Yao , Xubin Pan , Yuanyuan Dai , Yinghan Chen , Zepeng Chang , Zhangming Pei , Yue Xiao , Hongchao Wang , Wenwei Lu , Jianxin Zhao
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引用次数: 0

Abstract

Colitis is often accompanied with reduced intestinal α1,2-fucosylation. D-serine has been reported to prevent chronic colitis and upregulate the α1,2-fucosylation levels of intestinal epithelial cells in vitro. However, the role of D-serine in acute colitis and whether α1,2-fucosylation regulation is involved in the process remains unclear. In this study, D-serine alleviated body weight loss, colon shortening, and intestinal barrier damage in mice with acute colitis. Additionally, D-serine helped maintain gut microbiota balance by increasing the abundance of beneficial bacteria, including Bifidobacterium, and decreasing the harmful bacteria, such as Escherichia. Shigella. Furthermore, untargeted metabolomics showed that D-serine can modify the metabolism of cecal microbiota by decreasing concentrations of colitis-associated metabolites. Nevertheless, inhibiting α1,2-fucosylation impaired D-serine-mediated alleviation of colitis, highlighting the importance of α1,2-fucosylation upregulation in this process. D-serine significantly increased the trans-epithelial resistance of normal colonic epithelial cells, which was impaired by α1,2-fucosylation inhibition. Additionally, D-serine enhanced α1,2-fucosylation of macrophages (RAW264.7 cells) and reduced the secretion of tumor necrosis factor-α. The higher expression of the serine uptake gene Slc3a5 in type 3 innate lymphoid cells (ILC3s) suggested that D-serine may regulate intestinal α1,2-fucosylation by affecting IL-22 secretion of ILC3s. Taken together, our study showed that D-serine alleviates acute colitis by regulating α1,2-fucosylation of intestinal epithelial cells and macrophages. These findings suggest that regulating intestinal α1,2-fucosylation could be a potential strategy for the treatment of colitis.
D-丝氨酸通过调节肠道 α1,2-岩藻糖基化缓解结肠炎
结肠炎通常伴随着肠道α1,2-岩藻糖基化的减少。据报道,D-丝氨酸能预防慢性结肠炎,并能在体外上调肠上皮细胞的α1,2-岩藻糖基化水平。然而,D-丝氨酸在急性结肠炎中的作用以及α1,2-岩藻糖基化调节是否参与了这一过程仍不清楚。在这项研究中,D-丝氨酸减轻了急性结肠炎小鼠的体重下降、结肠缩短和肠屏障损伤。此外,D-丝氨酸还能增加有益菌(包括双歧杆菌)的数量,减少有害菌(如志贺氏菌)的数量,从而帮助维持肠道微生物群的平衡。志贺氏菌。此外,非靶向代谢组学研究表明,D-丝氨酸可以通过降低结肠炎相关代谢物的浓度来改变盲肠微生物群的代谢。然而,抑制α1,2-岩藻糖基化会削弱 D-丝氨酸介导的结肠炎缓解作用,这凸显了α1,2-岩藻糖基化上调在这一过程中的重要性。D-丝氨酸能明显增加正常结肠上皮细胞的跨上皮阻力,而抑制α1,2-岩藻糖基化则会削弱这种阻力。此外,D-丝氨酸还能增强巨噬细胞(RAW264.7 细胞)的α1,2-岩藻糖基化,减少肿瘤坏死因子-α的分泌。3型先天性淋巴细胞(ILC3s)中丝氨酸吸收基因Slc3a5的高表达表明,D-丝氨酸可能通过影响ILC3s的IL-22分泌来调节肠道α1,2-岩藻糖基化。综上所述,我们的研究表明,D-丝氨酸可通过调节肠上皮细胞和巨噬细胞的α1,2-岩藻糖基化来缓解急性结肠炎。这些发现表明,调节肠道α1,2-岩藻糖基化可能是治疗结肠炎的一种潜在策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Food Bioscience
Food Bioscience Biochemistry, Genetics and Molecular Biology-Biochemistry
CiteScore
6.40
自引率
5.80%
发文量
671
审稿时长
27 days
期刊介绍: Food Bioscience is a peer-reviewed journal that aims to provide a forum for recent developments in the field of bio-related food research. The journal focuses on both fundamental and applied research worldwide, with special attention to ethnic and cultural aspects of food bioresearch.
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