Resistant Maltodextrin Alleviates Dextran Sulfate Sodium-Induced Intestinal Inflammatory Injury by Increasing Butyric Acid to Inhibit Proinflammatory Cytokine Levels.

Shilan Wang,Zhenhua Wu,Junjun Wang,Shiyi Zhang,Yujun Wu,Shimeng Huang,Jiaman Pang,Dandan Han

doi:10.1155/2020/7694734

Shilan Wang, Zhenhua Wu + Show 6 more

Open Access

https://doi.org/10.1155/2020/7694734

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Journal: BioMed research international	Publication Date: Sep 16, 2020
Citations: 13	License type: CC BY 4.0

Affiliation: China Agricultural University

Abstract

Inflammatory bowel disease (IBD), one kind of intestinal chronic inflammatory disease, is characterized by colonic epithelial barrier injury, overproduction of proinflammatory cytokines, and fewer short-chain fatty acids (SCFAs). The present study is aimed at testing the hypothesis that resistant maltodextrin (RM), a soluble dietary fiber produced by starch debranching, alleviated dextran sulfate sodium- (DSS-) induced colitis in mice. Female C57BL/6 mice with or without oral administration of 50 mg/kg RM for 19 days were challenged with 3% DSS in drinking water to induce colitis (from day 14 to day 19). Although RM could not reverse DSS-induced weight loss or colon shortening, it reduced inflammatory cell infiltration and epithelial damage in colon tissue, as well as the transfer of intestinal permeability indicators including serum diamine oxidase (DAO) and D-lactic acid (D-LA). ELISA analysis indicated that RM significantly suppressed the increase of Th1 cytokines induced by DSS in the colon such as tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ). The levels of proinflammatory cytokines interleukin-1β (IL-1β), IL-17, and IL-8 in the DSS group were significantly higher than those in the control group and RM group, but no significant difference was observed in the RM-DSS group compared with the RM group. Interestingly, IL-10 levels of the DSS group were significantly higher than those of the other groups. With respect to SCFAs, DSS administration significantly decreased the concentration of faecal butyric acid while the RM-DSS group showed a tendency to increase (P = 0.08). In general, RM alleviated dextran sulfate sodium-induced intestinal inflammation through increasing the level of butyric acid and subsequently inhibiting the expression of proinflammatory cytokines.

Highlights

Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn disease (CD), is one of the intestinal chronic inflammatory diseases [1]
On the 3rd day after dextran sulfate sodium (DSS) treatment, disease activity index (DAI) scores were higher in the DSS group (P < 0:05, DSS vs. Resistant maltodextrin (RM)) than in the RM-DSS group (P > 0:05, RM-DSS vs. RM)
On the 4th day, DAI scores of the DSS group were significantly higher than those of the groups without DSS challenge (CON and RM groups) (P < 0:05), while there was no statistical difference between RM-DSS and groups without DSS challenge (CON and RM groups)

Summary

Introduction

Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn disease (CD), is one of the intestinal chronic inflammatory diseases [1]. The incidence and prevalence of IBD are on the rise worldwide [1]. Epithelial invasion of intestinal flora along with incomplete intestinal epithelial barriers is increasingly considered to have a causal relationship with IBD [2]. The gut inflammation occurring in patients with IBD is associated with excessive responses of Th1 or Th2 cells [3] and cytokines produced by Th17 cells [4]. In the mucosa and faeces of IBD patients, there were significantly fewer bacteria that can ferment fiber and produce shortchain fatty acids (SCFAs) than in healthy people [2]

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