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Inhibitory effect of Bifidobacterium bifidum ATCC 29521 on colitis and its mechanism
Ahmad Ud Din1, Adil Hassan2, Yuan Zhu2
1Key Laboratory for Bio-rheological Science and Technology of Ministry of Education, State and Local Joint Engineering Laboratory for Vascular Implants Bioengineering College of Chongqing University, Chongqing 400030, China; Drug Discovery Research Center, Southwest Medical University Luzhou, China.
Abstract:
Probiotics are known to be beneficial in preventing different diseases in model animals, including inflammatory bowel disease. However, there are few studies on probiotics related to miRNA regulation and disease status. In this article, the beneficial role and mechanisms of the probiotic strain Bifidobacterium bifidum ATCC 29521 have been studied in ulcerative colitis using dextran sodium sulphate (DSS) model. Male C57JBL/6 mice were randomly divided into three groups (n=7): Normal group, dextran sulphate sodium (DSS) group, and Bifido group gavage with Bifidobacterium bifidum ATCC 29521 (2×108 CFU/day). Our strain restored the DSS-caused damage by regulating the expression of immune markers and tight junction proteins (TJP) in the colon; briefly by up-regulating ROS-scavenging enzymes (SOD1, SOD2, CAT, and GPX2), anti-inflammatory cytokines (IL-10, PPARγ, IL-6), TJP's (ZO-1, MUC-2, Claudin-3, and E Cadherin-1) and downregulating inflammatory genes (TNF-α, IL-1β) in Bifido group mice. Inflammatory markers appeared to be regulated by NF-κB nuclear P65 subunit, and its translocation was inhibited in Bifido group mice colon. In addition, the expression of inflammatory genes and colonic TJP were also associated with the restoration of miRNAs (miR-150, miR-155, miR-223) in B. bifidum ATCC 29521 treated Bifido group. The dysbiosis executed by DSS was restored in the Bifido group, demonstrating that B. bifidum ATCC 29521 possessed a probiotic role in our DSS colitis mouse model. B. bifidum ATCC 29521 exhibited its probiotic role through its anti-inflammatory role by modulating miRNA-associated TJP and NF-κB regulation and by partially restoring dysbiosis.
Insights
Bifidobacterium bifidum ATCC 29521, a probiotic, mitigated ulcerative colitis in mice by regulating immune markers, tight junction proteins, and microRNAs. This strain offers a potential therapeutic strategy for inflammatory bowel disease.
Area of Science:
- Microbiology
- Immunology
- Gastroenterology
Background:
- Probiotics show promise in animal models for inflammatory bowel disease (IBD).
- Limited research exists on probiotic mechanisms involving microRNA (miRNA) regulation in disease.
- Ulcerative colitis (UC) is a chronic IBD with significant unmet therapeutic needs.
Purpose of the Study:
- To investigate the therapeutic effects and underlying mechanisms of Bifidobacterium bifidum ATCC 29521 in a mouse model of ulcerative colitis.
- To explore the role of this probiotic in regulating immune responses, tight junction proteins, and miRNA expression.
Main Methods:
- A dextran sodium sulphate (DSS)-induced colitis model in C57JBL/6 mice.
- Treatment groups included normal, DSS-induced colitis, and DSS-induced colitis gavaged with Bifidobacterium bifidum ATCC 29521.
- Analysis of immune markers, tight junction proteins (TJP), miRNA expression, and NF-κB pathway activation in colon tissue.
Main Results:
- Bifidobacterium bifidum ATCC 29521 administration restored DSS-induced colonic damage.
- The probiotic upregulated antioxidant enzymes, anti-inflammatory cytokines, and TJPs, while downregulating key inflammatory genes (TNF-α, IL-1β).
- NF-κB pathway activation was inhibited, and miRNA expression (miR-150, miR-155, miR-223) was restored in probiotic-treated mice.
Conclusions:
- Bifidobacterium bifidum ATCC 29521 demonstrates significant probiotic effects in a DSS-induced colitis model.
- The anti-inflammatory actions involve modulation of miRNA-associated TJPs and NF-κB signaling.
- This probiotic strain offers a potential therapeutic avenue for ulcerative colitis by restoring gut homeostasis and reducing inflammation.
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