Abstract
Background and AimsTo explore the inhibition mechanism of Saccharomyces boulardii (S. boulardii) on ulcerative colitis (UC) carcinogenesis.MethodsC57BL/6 mice were treated with azoxymethane and dextran sulfate sodium (AOM/DSS) to develop a UC carcinogenesis model. The treatment group was lavaged with S. boulardii (5 × 107 CFU/d) for 12 weeks. The mice were sacrificed and the tumor load in the treatment group was compared with that of a control group. The levels of TNF-α and IL-6 in colon tissue were measured by enzyme-linked immunosorbent assays. The influence of S. boulardii on TNF-α and IL-6 regulation was also investigated using different colon cell lines. Differences in intestinal microbiota in both stool and intestinal mucosa samples were assessed using 16S rDNA sequencing.ResultsS. boulardii treatment reduced AOM/DSS-induced UC carcinogenesis in mice, as indicated by the reduced tumor load and reduced TNF-α and IL-6 levels in vivo, as well its effects on TNF-α and IL-6 activities in vitro. Significant changes in both fecal and mucosal microbiota were observed among the control, the AOM/DSS treated, and AOM/DSS plus S. boulardii treated groups. For fecal microbiota, the AOM/DSS treated group was lower in Lactobacillus, but higher in Oscillibacter and Lachnoclostridium than the control group. After intervention with S. boulardii, the percentage of Bacillus and Lactococcus increased, but Lachnoclostridium, Oscillibacter, Bacteroides, and Pseudomonas decreased. For the intestinal mucosal microbiota, the AOM/DSS treated group was lower in Bifidobacterium and Ruminococcaceae_UCG-014 and higher in Alloprevotella than the control group. After S. boulardii exposure, the percentage contributions of Lachnoclostridium and Lachnospiraceae_NK4A136 increased.ConclusionsS. boulardii effectively reduced UC carcinogenesis in an AOM/DSS induced mice model. This positive result can likely be attributed to the reduction of TNF-α and IL-6 levels or the blockade of their function combined with alterations to the intestinal microbiota.
Highlights
Background and AimsTo explore the inhibition mechanism of Saccharomyces boulardii (S. boulardii) on ulcerative colitis (UC) carcinogenesis
Our results indicate that S. boulardii supplementation could alleviate UC carcinogenesis in mice through reducing levels of Tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) or impairing their function and altering the intestinal microbiota
Establishment of the UC carcinogenesis mice model through AOM/dextran sulfate sodium (DSS) treatment C57BL/6 mice were treated with AOM/DSS to establish a UC carcinogenesis mice model
Summary
To explore the inhibition mechanism of Saccharomyces boulardii (S. boulardii) on ulcerative colitis (UC) carcinogenesis. Ulcerative colitis (UC) is a chronic inflammatory disease of the colon [1]. Individuals with UC are at increased risk of developing colorectal cancer over healthy individuals [2]. One possible cause of UC carcinogenesis is repeated cycles of epithelial cell injury and repair [3]. During this process, cells are immersed in a chronic inflammatory cytokine milieu, with the overproduction of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6). IL-6 is another key cytokine that plays an important role in cancer progression [5]. Its pro-tumorigenic influence is largely mediated by the signal transducer and activator of transcription 3
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