Saccharomyces boulardii alleviates ulcerative colitis carcinogenesis in mice by reducing TNF-α and IL-6 levels and functions and by rebalancing intestinal ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-11-06

AUTHORS

Chunsaier Wang, Wenbin Li, Hongying Wang, Yiming Ma, Xinhua Zhao, Xudong Zhang, Hong Yang, Jiaming Qian, Jingnan Li

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. More... »

PAGES

246

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s12866-019-1610-8

DOI

http://dx.doi.org/10.1186/s12866-019-1610-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1122364288

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/31694526


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31 schema:description 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.
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39 Alloprevotella
40 Bacteroides
41 Bifidobacterium
42 DSS
43 IL-6
44 IL-6 activity
45 IL-6 levels
46 IL-6 regulation
47 Lachnoclostridium
48 Lactobacillus
49 Lactococcus
50 MethodsC57BL/6 mice
51 Oscillibacter
52 Pseudomonas
53 S. boulardii
54 Saccharomyces
55 TNF
56 UC carcinogenesis
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60 bacilli
61 background
62 blockade
63 boulardii
64 carcinogenesis
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66 cell lines
67 changes
68 colon cell lines
69 colon tissues
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73 dextran sulfate sodium
74 differences
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76 enzyme-linked immunosorbent
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78 fecal microbiota
79 function
80 group
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82 influence
83 inhibition mechanism
84 intervention
85 intestinal microbiota
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88 levels
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91 load
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93 mice
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97 mucosa samples
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99 percentage
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101 positive results
102 rDNA sequencing
103 reduction
104 reduction of TNF
105 regulation
106 results
107 samples
108 sequencing
109 significant changes
110 sodium
111 stool
112 sulfate sodium
113 tissue
114 treatment
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116 tumor load
117 vivo
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