Abstract

Background The relationship between inflammatory bowel disease and gut microbiota is inextricable. Electroacupuncture (EA) can alleviate acute experimental colitis, but the performance of intestinal microorganisms and the mechanism are still not fully understood. We investigated the relationship between the EA and gut microbes and clarified the role of tight junction and adiponectin in the anti-inflammatory effect of EA. Methods Male C57BL/6 mice were randomized into three groups: normal control, dextran sulfate sodium- (DSS-) induced ulcerative colitis (DSS), and DSS with EA ST36 (DSS + EA). Mice body weight, DAI score, colon length, and histological score were evaluated for colitis severity. Colonic inflammation and tight junctions were demonstrated by the immunohistochemical (IHC) method. Systemic responses were confirmed by plasma cytokines and adiponectin with multiplex immunoassays. Gut microbiome profiling was conducted by 16S rRNA gene sequencing. Results EA had benefit in relieving both macroscopic and microscopic colonic inflammation. It can reduce disease activity, maintain colon length, and ameliorate histological inflammatory reaction. In IHC stain, EA decreased CD11b, F4/80, TLR4, and MyD88 and preserved claudin-1 and ZO-1 expression. Compared with the control group, the DSS group showed elevated levels of CRP, IFN-γ, TNF-α, and IL-6, but decreased adiponectin. These changes were reversed by EA, accompanied by modulation of the overall structure of gut microbiota. Conclusion Our findings suggest that EA exerts its therapeutic effect by TLR4 signaling via the MyD88-dependent pathway. EA could increase adiponectin, maintain mucosal tight junctions, and modulate gut microbiota.

Highlights

  • Inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), result from chronic or relapsing immune activation and corresponding inflammation within the gastrointestinal tract. e prevalence of IBD in developed countries is more than in developing countries, which means genetic factors and environmental factors are involved [1]

  • Gut mucosal barrier dysfunction and translocation of gut microbiota are possible mechanisms of IBD, and the tight junction is the first line of defense [3]; even till there is no drug that could repair the tight junction in the gut mucosa

  • We demonstrated that repeated EA intervention ameliorates dextran sulfate sodium- (DSS-)induced colitis by suppressing proinflammatory mediators, including C-reactive protein (CRP), IFN-c, TNF-α, and IL-6 through the TLR4 signaling via MyD88-dependent pathway

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Summary

Introduction

Inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), result from chronic or relapsing immune activation and corresponding inflammation within the gastrointestinal tract. e prevalence of IBD in developed countries is more than in developing countries, which means genetic factors and environmental factors are involved [1]. Inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), result from chronic or relapsing immune activation and corresponding inflammation within the gastrointestinal tract. Gut mucosal barrier dysfunction (leaky gut) and translocation of gut microbiota are possible mechanisms of IBD, and the tight junction is the first line of defense [3]; even till there is no drug that could repair the tight junction in the gut mucosa. Acupuncture therapy has been one of the popular complementary and alternative medicines for many chronic diseases, including inflammatory bowel disease. Because IBD is a chronic relapsing-remitting disease of the gastrointestinal tract, more and more people choose complementary and alternative medicine for the IBD adjuvant therapy in the western world [4].

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