Selenium-enriched Bifidobacterium longum DD98 effectively ameliorates dextran sulfate sodium-induced ulcerative colitis in mice

Abstract

The pathogenesis of ulcerative colitis (UC) is complicated with impaired intestinal epithelial barrier and imbalanced gut microbiota. Both selenium and probiotics have shown effects in regulating intestinal flora and ameliorating UC. The objective of this study is to investigate the alleviating effects of Selenium-enriched Bifidobacterium longum DD98 (Se-B. longum DD98) on dextran sulfate sodium (DSS)-induced colitis in mice and explore the underlying mechanism. After treatment of B. longum DD98, Se-B. longum DD98, and sulfasalazine for 3 weeks, the disease severity of UC mice was decreased, with colon lengthened and pathological phenotype improved. The expression of pro-inflammatory cytokines and oxidative stress parameters were also decreased. Thus, Se-B. longum DD98 showed a stronger effect on relieving the aforementioned symptoms caused by DSS-induced colitis. Exploration of the potential mechanism demonstrated that Se-B. longum DD98 showed higher activities to suppress the inflammatory response by inhibiting the activation of the toll-like receptor 4 (TLR4), compared to B. longum DD98 and sulfasalazine. Se-B. longum DD98 also significantly improved the intestinal barrier integrity by increasing the expression of tight junction proteins including ZO-1 and occludin. 16S rDNA sequencing analyses showed that Se-B. longum DD98 improved the diversity of the intestinal flora and promoted the abundance of health-benefiting taxa including Lachnospiraceae, Lactobacillaceae, and Prevotellaceae in family level. In conclusion, compared to B. longum DD98 and sulfasalazine, Se-B. longum DD98 showed stronger therapeutic effects on DSS-induced colitis in mice and might be a promising candidate for the treatment of UC.

Bifidobacterium longum subsp. infantis FJSYZ1M3 ameliorates DSS-induced colitis by maintaining the intestinal barrier, regulating inflammatory cytokines, and modifying gut microbiota

“…26 And B. longum DD98 could increase the expression of tight junction protein in DSS-induced colitis, including ZO-1 and Occludin. 32 Moreover, the ameliorating effects of other Bifidobacterium strains on colitis showed to be related to their restoration of tight junction integrity, including B. breve , B. pseudocatenulatum , and B. bifidum . 21,27,33,34…”

Stronger gut microbiome modulatory effects by postbiotics than probiotics in a mouse colitis model

“…Differences in the gut microbiota modulatory effect between Bifidobacterium adolescentis B8598 and probiotic strains used in previous fecal microbiome-based studies in experimental colitis mouse model are summarized in Supplementary Table 5 19,22,25,29,31,32,[41][42][43][44][45] . Our results were similar to the observation of several previous reports that the phylum-level fecal microbiota did not show obvious changes subjected to probiotic supplementation 22,29,31,32,41,44 . Two studies identified significant changes in the species-level fecal microbiota.…”

Inflammatory Response: A Crucial Way for Gut Microbes to Regulate Cardiovascular Diseases

“…Clinically, the abuse of broad-spectrum antibiotics claims for the gastrointestinal barrier impairment via inhibiting the symbiotic bacteria, allows the infiltration of pathogenic bacteria and its detrimental metabolites into the circulation cycle. Conversely, increasing the number of probiotics is beneficial for gut microbiota function [ 61 ]. The Western diet (WD) is a crucial reason for systemic inflammation and cognitive decline in mice.…”