Abstract

This study aimed to investigate the protective effect of probiotics and synbiotics from traditional Thai fermented tea leaves (Miang) on dextran sulfate sodium (DSS)-induced colitis in mice, in comparison to sulfasalazine. C57BL/6 mice were treated with probiotics L. pentosus A14-6, CMY46 and synbiotics, L. pentosus A14-6 combined with XOS, and L. pentosus CMY46 combined with GOS for 21 days. Colitis was induced with 2% DSS administration for seven days during the last seven days of the experimental period. The positive group was treated with sulfasalazine. At the end of the experiment, clinical symptoms, pathohistological changes, intestinal barrier integrity, and inflammatory markers were analyzed. The probiotics and synbiotics from Miang ameliorated DSS-induced colitis by protecting body weight loss, decreasing disease activity index, restoring the colon length, and reducing pathohistological damages. Furthermore, treatment with probiotics and synbiotics improved intestinal barrier integrity, accompanied by lowing colonic and systemic inflammation. In addition, synbiotics CMY46 combined with GOS remarkedly elevated the expression of IL-10. These results suggested that synbiotics isolated from Miang had more effectiveness than sulfasalazine. Thereby, they could represent a novel potential natural agent against colonic inflammation.

Highlights

  • Ulcerative colitis (UC) is one of the most common types of inflammatory bowel disease (IBD) and is characterized by chronic and recurrent inflammatory conditions of the colon and rectum [1]

  • All treatments of probiotic and synbiotic for 21 days which were started 14 days before dextran sulfate sodium (DSS) administration did not result in any sign of toxicity

  • Mice received 2% DSS administration in drinking water for seven days continuously after day fourteen, resulting in colonic inflammation as demonstrated by body weight loss and a high score of DAI compared to the normal group (Figure 2a,b)

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Summary

Introduction

Ulcerative colitis (UC) is one of the most common types of inflammatory bowel disease (IBD) and is characterized by chronic and recurrent inflammatory conditions of the colon and rectum [1]. The pathogenesis of UC involves interplay of multifactorial factors, including genetic susceptibility, environmental factors, and gut microbiota, triggering the dysregulation of gut barrier function and immune-related inflammation response [3]. The colonic damages in UC patients are driven by the immune cells and cytokines response. The progression of UC has indicated that proinflammatory cytokines including interleukin (IL)-1, IL-6, IL-9, IL-13, IL-33, and tumor necrosis factor-α (TNF-α) are usually upregulated, whereas anti-inflammatory cytokines including transforming growth factor-β (TGF-β), IL-10, and IL-37 are downregulated [4]. Intestinal barrier disruption during mucosal inflammation is involved in impairing structure and remodeling of apical junctions, leading to increase gut permeability and systemic inflammation-related diseases [3]. The conventional therapeutic drugs for UC, such as anti-inflammatory, antibiotics, and immunosuppressant drugs have adverse side effects and are limited in their benefits [5]. There is a need to explore and develop novel alternative therapeutics to reduce and counter complications and the negative symptoms from medications in UC patients

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