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膳食中的κ-卡拉胶会促进肠道微生物群介导的肠道炎症。

Dietary κ-carrageenan facilitates gut microbiota-mediated intestinal inflammation.

作者信息

Wu Wei, Zhou Jiawei, Xuan Rongrong, Chen Juanjuan, Han Hui, Liu Jingwangwei, Niu Tingting, Chen Haimin, Wang Feng

机构信息

State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products, Ningbo University, Ningbo, China; Collaborative Innovation Center for Zhejiang Marine High-efficiency and Healthy Aquaculture, Ningbo University, Ningbo, Zhejiang 315211, China.

Department of Gynecology and Obstetrics, the Affiliated Hospital of Medical College of Ningbo University, Ningbo, Zhejiang 315211, China.

出版信息

Carbohydr Polym. 2022 Feb 1;277:118830. doi: 10.1016/j.carbpol.2021.118830. Epub 2021 Nov 2.

DOI:10.1016/j.carbpol.2021.118830
PMID:34893247
Abstract

The inflammatory effects of carrageenan (CGN), a ubiquitous food additive, remains controversial. Gut microbiota and intestinal homeostasis may be a breakthrough in resolving this controversy. Here we show that, κ-CGN did not cause significant inflammatory symptoms, but it did cause reduced bacteria-derived short-chain fatty acids (SCFAs) and decreased thickness of the mucus layer by altering microbiota composition. Administration of the pathogenic bacterium Citrobacter rodentium, further aggravated the inflammation and mucosal damage in the presence of κ-CGN. Mucus layer degradation and altered SCFA levels could be reproduced by fecal transplantation from κ-CGN-fed mice, but not from germ-free κ-CGN-fed mice. These symptoms could be partially repaired by administering probiotics. Our results suggest that κ-CGN may not be directly inflammatory, but it creates an environment that favors inflammation by perturbation of gut microbiota composition and then facilitates expansion of pathogens, and this effect may be partially reversed by the introduction of probiotics.

摘要

角叉菜胶(CGN)是一种普遍存在的食品添加剂,其炎症效应仍存在争议。肠道微生物群和肠道内稳态可能是解决这一争议的突破口。在此我们表明,κ-CGN不会引起明显的炎症症状,但它确实会通过改变微生物群组成导致细菌衍生的短链脂肪酸(SCFA)减少以及黏液层厚度降低。致病性鼠柠檬酸杆菌的施用在κ-CGN存在的情况下进一步加剧了炎症和黏膜损伤。黏液层降解和SCFA水平改变可通过来自喂食κ-CGN小鼠的粪便移植重现,但无菌喂食κ-CGN小鼠的粪便移植则不会。通过施用益生菌可部分修复这些症状。我们的结果表明,κ-CGN可能不会直接引发炎症,但它会通过扰乱肠道微生物群组成创造有利于炎症的环境,进而促进病原体的扩张,并且引入益生菌可能会部分逆转这种效应。

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