Lactobacillus reuteri Ameliorates Intestinal Inflammation and Modulates Gut Microbiota and Metabolic Disorders in Dextran Sulfate Sodium-Induced Colitis in Mice.

Gang Wang,Xiangfang Zeng,Shiyan Qiao,Yuming Wang,Shuo Huang,Haitao Yu,Shuang Cai

doi:10.3390/nu12082298

Gang Wang, Xiangfang Zeng + Show 5 more

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https://doi.org/10.3390/nu12082298

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Journal: Nutrients	Publication Date: Jul 31, 2020
Citations: 54	License type: CC BY 4.0

Affiliation: China Agricultural University

Abstract

Lactobacillus reuteri, a commensal intestinal bacteria, has various health benefits including the regulation of immunity and intestinal microbiota. We examined whether L. reuteri I5007 could protect mice against colitis in ameliorating inflammation, modulating microbiota, and metabolic composition. In vitro, HT-29 cells were cultured with L. reuteri I5007 or lipopolysaccharide treatment under three different conditions, i.e., pre-, co- (simultaneous), and posttreatment. Pretreatment with L. reuteri I5007 effectively relieves inflammation in HT-29 cells challenged with lipopolysaccharide. In vivo, mice were given L. reuteri I5007 by gavage throughout the study, starting one week prior to dextran sulfate sodium (DSS) treatment for one week followed by two days without DSS. L. reuteri I5007 improved DSS-induced colitis, which was confirmed by reduced weight loss, colon length shortening, and histopathological damage, restored the mucus layer, as well as reduced pro-inflammatory cytokines levels. Analysis of 16S rDNA sequences and metabolome demonstrates that L. reuteri I5007 significantly alters colonic microbiota and metabolic structural and functional composition. Overall, the results demonstrate that L. reuteri I5007 pretreatment could effectively alleviate intestinal inflammation by regulating immune responses and altering the composition of gut microbiota structure and function, as well as improving metabolic disorders in mice with colitis.

Highlights

The incidence and prevalence of inflammatory bowel disease (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), has steadily increased over time in recent decades, especially in many newly industrialized countries [1,2]
The precise etiology of IBD remains unknown, there are some cases reporting that environmental factors and genetic susceptibilities contribute to dysfunctions of the intestinal epithelial barrier, and this is associated with dysbiosis of the gut microbiota and mucosal inflammation [3]
We subsequently demonstrated the effects of L. reuteri I5007 pretreatment on colonic inflammation, colonic microbiota composition, and metabolic pathways in a dextran sulfate sodium (DSS)-induced mouse model of colitis

Summary

Introduction

The incidence and prevalence of inflammatory bowel disease (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), has steadily increased over time in recent decades, especially in many newly industrialized countries [1,2]. Accumulating evidence has shown that microbial dysbiosis plays a crucial role in the pathogenesis of IBD by affecting the metabolic pathway, intestinal barrier, and gut immunity [4]. Significant differences, such as reduced diversity and bacterial load, have been observed between the microbiota of patients with IBD and those of healthy individuals [5,6]. Beneficial bacterial species may protect the host mucosa from unwarranted and potentially harmful inflammatory responses [7,8]. The therapeutic modulation of imbalanced gut microbiota has been widely used for the treatment of IBD and has been proven to be a promising approach to therapy with significant clinical efficacy [10]

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