This was a pilot study aiming to evaluate the effects of probiotics as adjunctive treatment for ulcerative colitis (UC). Twenty-five active patients with UC were assigned to the probiotic (n = 12) and placebo (n = 13) groups. The probiotic group received mesalazine (60 mg kg À1 day À1) and oral probiotics (containing Lactobacillus casei Zhang, Lactobacillus plantarum P-8 and Bifidobacterium animalis subsp. lactis V9) twice daily for 12 weeks, while the placebo group received the same amounts of mesalazine and placebo. The clinical outcomes were assessed. The gut mucosal microbiota was profiled by PacBio single-molecule, real-time (SMRT) sequencing of the full-length 16S rRNA of biopsy samples obtained by colonoscopy. A significantly greater magnitude of reduction was observed in the UC disease activity index (UCDAI) in the probiotic group compared with the placebo group (P = 0.043), accompanying by a higher remission rate (91.67% for probiotic-receivers versus 69.23% for placebo-receivers, P = 0.034). The probiotics could protect from diminishing of the microbiota diversity and richness. Moreover, the gut mucosal microbiota of the probiotic-receivers had significantly more beneficial bacteria like Eubacterium ramulus (P < 0.05), Pediococcus pentosaceus (P < 0.05), Bacteroides fragilis (P = 0.02) and Weissella cibaria (P = 0.04). Additionally, the relative abundances of the beneficial bacteria correlated significantly but negatively with the UCDAI score, suggesting that the probiotics might alleviate UC symptoms by modulating the gut mucosal microbiota. Our research has provided new insights into the mechanism of symptom alleviation in UC by applying probiotic-based adjunctive treatment.
Alcoholic liver disease (ALD) is a liver disease caused by long-term heavy drinking, which is characterized by increased inflammation and oxidative stress in the liver and gut dysbiosis. The purpose of this study was to investigate the protective effect of administering ordinary and probiotic-(containing the Bifidobacterium animalis ssp. lactis Probio-M8 strain; M8) fermented milk to rats. Several biochemical parameters and the fecal metagenomes were monitored before (d 0) and after (d 42) the intervention. Our results confirmed that alcohol could cause significant changes in the liver levels of the proinflammatory cytokine IL-1β, antioxidation indicators, and liver function-related indicators; meanwhile, the gut bacterial and viral microbiota were disrupted with significant reduction in microbial diversity and richness. Feeding the rats with Probio-M8-fermented milk effectively maintained the gut microbiota stability, reduced liver inflammation and oxidative stress, and mitigated liver damages in ALD. Moreover, the Probio-M8-fermented milk reversed alcohol-induced dysbiosis by restoring the gut microbiota diversity, richness, and composition. Four predicted fecal metabolites (inositol, tryptophan, cortisol, and vitamin K2) increased after the intervention, which might help regulate liver metabolism and alleviate ALD-related symptoms. In short, our data supported that consuming Probio-M8-fermented milk effectively mitigated ALD. The protective effect against ALD could be related to changes in the gut microbiome after probiotic-fermented milk consumption. However, such observation and the causal relationship among probiotic milk consumption, changes in gut microbiome, and disease alleviation would still need to be further confirmed. Nevertheless, this study has shown in a rat model that consuming probiotic-fermented milk could protect against ALD.
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