Abstract

Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD) with a complex aetiology that commonly recurs. Most drugs for UC treatment interfere with metabolism and immune responses, often causing some serious adverse reactions. Therefore, the development of alternative treatments, including nutritional supplements and probiotics, have been one of the main areas of current research due to fewer side effect. As both a Chinese medicine and a food, edible bird’s nest (EBN) has high nutritional value. Modern pharmacological studies have shown that it has anti-inflammatory, immunoregulatory, antiviral and neuroprotective effects. In this study, UC was induced with dextran sulfate sodium (DSS) to investigate the protective effect of EBN on colitis mice and the related mechanism. The body weight, faecal morphology and faecal occult blood results of mice were recorded every day from the beginning of the modelling period. After the end of the experiment, the length of the colon was measured, and the colon was collected for histopathological detection, inflammatory factor detection and immunohistochemical detection. Mouse spleens were dissected for flow cytometry. The results showed that in mice with colitis, EBN improved symptoms of colitis, reduced colonic injury, and inhibited the increases in the levels of the pro-inflammatory cytokines IL-1β and TNF-α. The T helper 17 (Th17)/regulatory T (Treg) cell balance was restored by decreasing the expression of IL-17A and IL-6 in intestinal tissues, increasing the expression of TGF-β, and decreasing the number of Th17 cells in each EBN dose group. These findings suggest that EBN has a protective effect on DSS-mediated colitis in mice, mainly by restoring the Th17/Treg cell balance.

Highlights

  • Ulcerative colitis (UC) is a major form of inflammatory bowel disease (IBD) characterized by recurring and diffuse inflammation in the rectal and colonic mucosa

  • These results suggest that edible bird’s nest (EBN) can alleviate the clinical symptoms of UC and could be a latent drug for UC

  • In comparison with modelling alone, EBN pretreatment dramatically inhibited the overexpression of IL-17A and Foxp3 induced by dextran sulfate sodium (DSS) (Figure 6). These results indicated that the counts of T helper 17 (Th17) cells and Treg cells in the colon could be restored to a normal balance, which was consistent with the results for the spleen

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Summary

Introduction

Ulcerative colitis (UC) is a major form of inflammatory bowel disease (IBD) characterized by recurring and diffuse inflammation in the rectal and colonic mucosa. As an important public health problem and a global disease, UC tends to affect young people, which could increase the risk of colorectal cancer (Feuerstein et al, 2019). Risk factors for the development of UC are related to disruption of the intestinal mucosal barriers, which can be caused by infections, medications or familial genetics. Chronic and relapsing immune responses and clinical symptoms seriously reduce the quality of life of patients with UC. As a result of its complicated pathogenesis, UC has not yet been cured, and the goal of therapy in UC is to first induce clinical remission and achieve steroid-free maintenance of remission (Feuerstein et al, 2019). There is an urgent need to develop novel therapeutic approaches for UC patient treatment

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