Soaring incidence of UC

Ulcerative colitis (UC) is a subtype of inflammatory bowel diseases (IBD), characterized as abdominal pain, diarrhea, and blood stool. UC occurs all over the world with a rapidly increasing morbidity due to accelerating circadian rhythm and actuating pressure. Conventional therapies for UC, including aminosalicylate, antibiotics, steroids, immunomodulators and biological applications, have achieved stable management for some patients. Unfortunately, severe adverse reactions like infection and renal injury can not be ignored. It is reported that UC can induce harmful effects on human health, and the relapse-remission cycles and incurable have made it a high-risk factor for colorectal cancer initiation and development.

Saccharomyces boulardii Bld-3 exerts protective effects on colitis in mice

Saccharomyces boulardii Bld-3 has shown a clinically beneficial effect in inflammatory bowel diseases recently. However, the underlying mechanisms remain incompletely understood. So we conducted a study to tested whether S. boulardii Bld-3 targets gut microbiota to protect against the development of experimental colitis in mice.

In our research, female C57BL/6 mice were gavaged with S. boulardii Bld-3 for 3 weeks before being challenged with dextran sulphate sodium to induce ulcerative colitis. Bodyweight, diarrhea severity, intestinal permeability, colonic histopathology, colonic inflammatory status, and epithelial cell death of mice were examined.The fecal microbiota and its metabolomic profiles were detected by 16S rDNA sequencing and UPLC-MS, respectively.

The result showed that S. boulardii Bld-3 pretreatment mitigated the classic symptoms of acute colitis in mice, involving up-regulated body weight and colon length, while down-regulated the DAI score.

Supplementation with S. boulardii significantly prevented weight loss and colon shortening, lowered colonic inflammation, ameliorated epithelial injury, and enhanced the intestinal barrier integrity in colitis mice. By inhibiting the abundance of pathogenic bacteria and increasing the probiotics abundance, S. boulardii improved the microbial diversity and restored the microbiota dysbiosis. The excessive cell apoptosis in colitis tissue, as a result of hyperinflammatory response, was also alleviated by S. boulardii treatment. Another symptom of UC is intestinal epithelial barrier damage, which may further lead to bacterial translocation and other antigens’ entrance. The tight junction proteins, ZO-1 and occluding, are indicative of the epithelial integrity and junction stability, respectively. Both are generally considered as markers of epithelial barrier function. Pre-treatment of S. boulardii Bld-3 improved the epithelial integrity by enhancing ZO-1 and occludin expression, demonstrating that S. boulardii Bld-3 exerts efficient protection and repairment on the intestinal epithelium through various paths.

Gut microbiota has long been regarded as an important component of intestinal barrier, which is pivotal in the pathogenesis of DSS-induced colitis. This research found that DSS-induced colitis mice manifested a lower α-diversity and a distintive β-diversity compared to the control mice. The differences were driven by a reduction in the relative abundance of Bacteroidetes and an elevation in Firmicutes and Verrucomicrobia at the phylum level. Importantly, after S. boulardii Bld-3 treatment, the gut microbiota diversity of colitis mice was improved and the community composition was similar to the control.

Moreover, it also modulated the microbial metabolome and altered the relative contents of metabolites involving amino acids, lipids, energy and vitamin metabolisms. These yeast-driven shifts in gut flora and metabolites are were associated with each other and with the inflammation profile in colitis.

Collectively, S. boulardii Bld-3 exerts protective effects on colitis in mice by reshaping gut microbiome and its metabolic profile, indicating it as a promising therapeutic avenue.

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