Saccharomyces cerevisiae I4 Showed Alleviating Effects on Dextran Sulfate Sodium-Induced Colitis of Balb/c Mice

Abstract

Ulcerative colitis (UC) is a chronic inflammatory bowel disease. The purpose of this study was to investigate the ameliorating effects of three yeast strains, Saccharomyces cerevisiae I4, Clavispora lusitaniae 30 and Pichia kudriavzevii 11, isolated from traditional fermented dairy food in Xinjiang, China, on the ulcerative colitis symptoms of Balb/c mice treated by dextran sulfate sodium (DSS). Among which, S. cerevisiae I4 had good tolerance to simulated gastrointestinal juice and strong adhesion to HT−29 cells monolayers. Furthermore, the three yeast strains were oral administered to Balb/c mice with DSS induced colitis. The weight loss, colon shortening and histological injury of colitis mice were ameliorated. Then, oral administration of S. cerevisiae I4 improved the immune state by reducing the contents of TNF−α, IL−6 and IL−1β and increasing immunoglobulin. The relative expression of intestinal barrier proteins Claudin−1, Occludin and Zonula Occludins−1 (ZO−1) of the mice enhanced, and the short chain fatty acids (SCFAs) content such as Propionic acid, Butyric acid, Isobutyric acid and Isovaleric acid in the feces of the mice increased to varying degrees, after S. cerevisiae I4 treatment compared with the model group of drinking 3% DSS water without yeast treatment. Moreover, S. cerevisiae I4 treatment lifted the proportion of beneficial bacteria such as Muribaculaceae, Lactobacillaceae and Rikenellaceae in the intestinal tract of the mice, the abundance of harmful bacteria such as Staphylococcus aureus and Turicibacter was decreased. These results suggested that S. cerevisiae I4 could alleviate DSS induced colitis in mice by enhancing intestinal barrier function and regulating intestinal flora balance.

Anti-Inflammatory, Barrier Maintenance, and Gut Microbiome Modulation Effects of Saccharomyces cerevisiae QHNLD8L1 on DSS-Induced Ulcerative Colitis in Mice

“…After yeast intervention, the relative abundance of Proteobacteria decreased, and that of Firmicutes increased to some degree ( Figure 7 ). Therefore, these yeasts reduced the microbiota structure imbalance, which is consistent with the results of a previous study [ 30 ].…”

“…S. boulardii CNCMI-745 and S. cerevisiae QHNLD8L1 significantly increased the relative expression levels of Claudin-1 and Occludin ( Figure 1 ). Similar to our results, S. cerevisiae I4 significantly upregulated these two genes in HT-29 cell monolayers [ 30 ]. Mu et al showed that yeast metabolites promoted RAW264.7 macrophage proliferation and reduced NO production [ 10 ].…”

“…The yeast adhesion capacity was evaluated using a modified method similar to that used by Meng et al [ 30 ]. Human colon cell line HT-29 was purchased from American Type Culture Collection (Manassas, VA, USA).…”

Ameliorative Effect of Saccharomyces cerevisiae JKSP39 on Fusobacterium nucleatum and Dextran Sulfate Sodium-Induced Colitis Mouse Model

“…F. nucleatum could upregulate the canonical NF-κB pathway and increase the expression of proinflammatory cytokines, such as IL-6, IL-17F, TNF-α, IL-12, IL-21, and IL-22, all of which could promote triggering the colonic inflammation and carcinogenesis. , A decrease in the Bcl-2/Bax ratio can lead to an exacerbate disturbance in intestinal homeostasis and apoptosis. In this study, the expression of Bcl-2 was remarkably decreased (Figure A,F,H), and the Bax was increased after treatment with Fn and DSS at RNA and protein levels (Figure B,G,H).…”

“…cerevisiae in the colonic fungal flora of patients with colorectal cancer and IBD was lower than that of healthy subjects. , Other studies showed that supplementation with S. cerevisiae could alleviate DSS-induced colitis mice by downregulating the expression of proinflammatory cytokine (TNF-α), myeloperoxidase, and eosinophil peroxidase activities, regulating gut microbiota, and enhancing the intestinal barrier. , However, few studies have systematically investigated the mechanism by which S. cerevisiae intervenes in Fn-involved IBD by improving oxidative stress and regulating the gut microbiota.…”