Abstract

Inflammatory bowel disease (IBD) is a group of conditions involving chronic relapsing-remitting inflammation of the gastrointestinal tract with an unknown etiology. Although the cause–effect relationship between gut microbiota and IBD has not been clearly established, emerging evidence from experimental models supports the idea that gut microbes play a fundamental role in the pathogenesis of IBD. As microbiome-based therapeutics for IBD, the beneficial effects of probiotics have been found in animal colitis models and IBD patients. In this study, based on the dextran sulfate sodium (DSS)-induced colitis mouse model, we investigated Lactobacillus rhamnosus strain LDTM 7511 originating from Korean infant feces as a putative probiotic strain for IBD. The strain LDTM 7511 not only alleviated the release of inflammatory mediators, but also induced the transition of gut microbiota from dysbiotic conditions, exhibiting the opposite pattern in the abundance of DSS colitis-associated bacterial taxa to the DSS group. Our findings suggest that the strain LDTM 7511 has the potential to be used as a probiotic treatment for IBD patients in comparison to L. rhamnosus GG (ATCC 53103), which has been frequently used for IBD studies.

Highlights

  • Inflammatory bowel disease (IBD) is an idiopathic chronic disease that involves inflammation of the gastrointestinal (GI) tract, including Crohn’s disease (CD) and ulcerative colitis (UC) [1]

  • Zhai et al [49] reported that the administration of two strains of the next-generation probiotic Akkermansia muciniphila displayed strain-specific characteristics in alleviating dextran sulfate sodium (DSS) chronic colitis, which were attributed to genetic differences between the two strains

  • L. rhamnosus ATCC 53103 (LGG) is a commensal bacterium isolated from a healthy human GI tract in 1983 [50]

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Summary

Introduction

Inflammatory bowel disease (IBD) is an idiopathic chronic disease that involves inflammation of the gastrointestinal (GI) tract, including Crohn’s disease (CD) and ulcerative colitis (UC) [1]. Despite numerous studies and research, a definitive pathogenesis of IBD has not yet been elucidated. Scientific evidence has shown that IBD is driven by genetic defects and environmental factors [3], and the collapse of the mucosal barrier function could trigger the penetration of gut pathobionts into the mucosa, resulting in inflammation responses [4,5]. The role of gut microbiota in the pathogenesis of IBD has been focused on, and in particular, studies in germ-free mice have revealed that gut bacteria are essential for the initiation of intestinal inflammation [6]. Whether the gut microbiota represent the cause or correlation of IBD has been a controversial topic [7,8]. Microbiome-based therapeutics, such as prebiotics, probiotics, postbiotics, and fecal microbiota transplantation (FMT), have been proposed as promising strategies for IBD treatment [9]

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