ArticleJournal of gastroenterology2026
Bifidobacterium bifidum CIP-01 attenuates metabolic dysfunction-associated steatotic liver disease induced by high-alcohol-producing Klebsiella pneumoniae.
Article in Journal of gastroenterology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Metabolic dysfunction-associated steatotic liver disease: pathogenic mechanisms and exercise-induced molecular adaptations.Lipids in health and disease · 2026Review
- Potential mechanisms by which microbiota-accessible carbohydrates regulate hepatic lipid metabolism in MAFLD via the gut-liver axis.Frontiers in microbiology · 2026Review
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Authors and funding
19 authors.
Funding
Abstract
backgroundHigh-alcohol-producing Klebsiella pneumoniae (HiAlc Kpn) can cause metabolic dysfunction-associated steatotic liver disease (MASLD) through sustained alcohol overflow in the microenvironment. As a probiotic, Bifidobacterium bifidum (B. bifidum) exhibits unique anti-inflammatory properties; however, whether and how it alleviate MASLD induced by HiAlc Kpn requires further investigation.
methodsMASLD mouse model was constructed by gavage administration with HiAlc Kpn W14 to assess the therapeutic effect of B. bifidum CIP-01 in vivo. Cell infection models, metabolomics sequencing, and in vitro antibacterial assays were integrated to systematically elucidate the mechanism by which B. bifidum CIP-01 mitigates HiAlc Kpn W14-induced cell damage.
resultsB. bifidum CIP-01 was able to ameliorate MASLD induced by HiAlc Kpn through a multi-target mechanism. Compared to pair-fed mice, HiAlc Kpn W14 disrupted gut barrier and promoted inflammatory cytokines release. While, supplementation with B. bifidum CIP-01 reversed these effects by a) restoring intestinal integrity via upregulating tight junction proteins (ZO-1/Occludin) and mucin protein MUC-2, reducing reactive oxidative stress (ROS) and apoptosis in colonic cells, and b) rescuing hepatic cytochrome P450 2E1 (CYP2E1)-driven oxidative injury (ROS/Caspase-3) while promoting mitochondrial β-oxidation, as well as c) directly suppressing HiAlc Kpn proliferation and biofilm formation. Metabolomics and 16S rRNA of fecal samples analyses revealed B. bifidum CIP-01-mediated metabolic regulation: depletion of toxic branched-chain amino acids (BCAAs) intermediates and restoration of energy homeostasis and antioxidant defense alongside increased short-chain fatty acids (SCFAs)-associated pathways.
conclusionOur findings highlight B. bifidum CIP-01 as a novel therapeutic candidate for HiAlc Kpn-induced MASLD, operating through a triad of pathogen suppression, gut-liver axis repair, and metabolic regulation.
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