Fructooligosaccharide supplementation alleviated the pathological immune response and prevented the impairment of intestinal barrier in DSS-induced acute colitis mice

低聚果糖 失调 免疫系统 炎症性肠病 结肠炎 肠道菌群 合生元 炎症 肠粘膜 生物 医学 益生元 免疫学 内科学 疾病 益生菌 细菌 食品科学 遗传学
作者
Minjing Liao,Yuanfang Zhang,Yilan Qiu,Zhengchun Wu,Zhihong Zhong,Xiaoqi Zeng,Yiliang Zeng,Li Xiong,Yu Wen,Rushi Liu
出处
期刊:Food & Function [The Royal Society of Chemistry]
卷期号:12 (20): 9844-9854 被引量:37
标识
DOI:10.1039/d1fo01147b
摘要

The dysbiosis of gut microbiota is closely related to the occurrence and development of inflammatory bowel disease (IBD). The manipulation of intestinal flora through prebiotics or probiotics is expected to induce and maintain the remission of IBD symptoms. 6-week-old C57BL/J mice were daily gavaged with fructooligosaccharides (FOS) or the synbiotic two weeks before the administration of dextran sulfate sodium (DSS). The supplementation of FOS or synbiotic could significantly ameliorate the body weight loss and colon histological damage in DSS-induced acute colitis mice. The altered composition of gut microbiota in acute colitis mice was reversed by FOS or Synbiotic supplementation, with a characteristic of decreased abundance of Mucispirillum. Both FOS and synbiotic mitigated DSS-induced loss of mucus protein (MUC2) and epithelium tight junction proteins (ZO-1, Occluding, Claudin1) in colon mucosa. The expression of pro-inflammatory cytokines (IL-6 and TNF-α) was decreased by FOS or synbiotic treatment, while the expression of Tbx21 and IL-10 was increased. The results suggested that the modulation of gut microbiota by FOS or synbiotic supplementation could decrease the inflammation potential of colonized commensals, which prevented the impairment of the intestinal barrier and induced a regulation of immune response in DSS-induced acute colitis mice.
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