Wu Dongmei, Ye Xingqian, Hu Weiwei, Yu Chengxiao, Zhu Kai, Pan Haibo, Chen Jianle, Cheng Huan, Chen Shiguo
College of Biosystems Engineering and Food Science, National-Local Joint Engineering Laboratory of Intelligent Food Technology and Equipment, Zhejiang Key Laboratory for Agro-Food Processing, Integrated Research Base of Southern Fruit and Vegetable Preservation Technology, Zhejiang International Scientific and Technological Cooperation Base of Health Food Manufacturing and Quality Control, Zhejiang University, Hangzhou 310058, China.
Food Funct. 2025 Jan 20;16(2):657-672. doi: 10.1039/d4fo03363a.
Inflammatory bowel diseases (IBDs), including Crohn's disease (CD) and ulcerative colitis (UC), are chronic conditions characterized by periods of intestinal inflammation and have become global diseases. Dietary pectins have shown protective effects on IBD models. However, the development of pectin-based diet intervention for IBD individuals requires knowledge of both the bioactive structural patterns and the mechanisms underlying diet-microbiota-host interactions. Here, dextran sulfate sodium (DSS) induced colitis mice were fed with different pectins with various domain compositions, including AG, P37, P55 and P85, in order to understand why different structural patterns function differently on colitis mouse models. The structural diversity of pectin manifests in the different percentages of the homogalacturonan (HG) backbone, Ara sidechains, and Gal sidechains. AG comprises only neutral sugar chains consisting of 14% Ara and 86% Gal, and P85 is a commercial HG pectin mainly composed of 85% HG. P37 and P55 were isolated from raspberry pulps with different domain ratios (P37 = 37% HG + 22% Ara + 32% Gal; P55 = 55% HG + 16% Ara + 18% Gal). Compared to the monotonous structure of AG and P85, the domain-diverse pectins P37 and P55 show superior protective effects against colitis through inhibiting the proliferation of the mucin-consuming bacteria and the pro-inflammatory microorganisms, potentiating the expression and the mucus layer and regulating the gut-spleen axis. The HG structure promoted the proliferation of the mucin-degrading microbiota and potentiated mucus erosion. AG enhanced the mucus thickness but increased the growth of the pro-inflammatory microbiota. Our study revealed that the specific domain composition of pectic fibers was a key factor on which the diet-induced alterations in the gut microbiota and the intestinal barrier function highly depended.
炎症性肠病(IBD),包括克罗恩病(CD)和溃疡性结肠炎(UC),是一种以肠道炎症反复发作为特征的慢性疾病,现已成为全球性疾病。膳食果胶已被证明对IBD模型具有保护作用。然而,针对IBD患者开发基于果胶的饮食干预措施,需要了解生物活性结构模式以及饮食-微生物群-宿主相互作用的潜在机制。在此,为了弄清楚为何不同的结构模式在结肠炎小鼠模型上发挥不同的作用,给硫酸葡聚糖钠(DSS)诱导的结肠炎小鼠喂食了具有不同结构域组成的不同果胶,包括AG、P37、P55和P85。果胶的结构多样性体现在同型半乳糖醛酸聚糖(HG)主链、阿拉伯糖侧链和半乳糖侧链的不同比例上。AG仅由中性糖链组成,其中阿拉伯糖占14%,半乳糖占86%,P85是一种商业HG果胶,主要由85%的HG组成。P37和P55是从树莓果肉中分离出来的,具有不同的结构域比例(P37 = 37% HG + 22%阿拉伯糖 + 32%半乳糖;P55 = 55% HG + 16%阿拉伯糖 + 18%半乳糖)。与AG和P85单一的结构相比,具有不同结构域的果胶P37和P55通过抑制消耗粘蛋白的细菌和促炎微生物的增殖、增强粘蛋白的表达和黏液层以及调节肠-脾轴,对结肠炎表现出更好的保护作用。HG结构促进了降解粘蛋白的微生物群的增殖,并加剧了黏液侵蚀。AG增加了黏液厚度,但促进了促炎微生物群的生长。我们的研究表明,果胶纤维的特定结构域组成是饮食诱导的肠道微生物群和肠道屏障功能改变高度依赖的关键因素。