ArticleCellular and molecular gastroenterology and hepatology2026
Microbial Monotherapy With Leuconostoc sp LB-P8 Improves Inflammation and Fibrosis in Mouse Primary Sclerosing Cholangitis by Inhibiting Transforming Growth Factor β1/SMAD Signaling.
Article in Cellular and molecular gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- From Kimchi to Primary Sclerosing Cholangitis: Leuconostoc citreum LB-P8 as a Microbiome-Based Therapeutic Approach.Cellular and molecular gastroenterology and hepatology · 2026Article
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9 authors.
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No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsPrimary sclerosing cholangitis (PSC) is a prototypical disease with an impaired gut-liver axis, frequently associated with inflammatory bowel disease, and linked to microbial dysbiosis. However, how microbes influence PSC progression remains unclear. We identified a novel L sp. (LB-P8) with potential anti-fibrotic properties via inhibition of transforming growth factor beta-1 (TGF-β)/SMAD signaling and investigated its therapeutic efficacy and mechanisms in mouse PSC models.
methodsHuman intestinal cells were cultured with or without LB-P8 to assess metabolite profiles (untargeted ultra-performance liquid chromatography-tandem mass spectrometry) and gene expression in co-cultured myofibroblasts and macrophages (reverse transcription-quantitative polymerase chain reaction). LB-P8 was orally gavaged following disease onset in three cholestatic models: bile duct ligation (BDL), 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) feeding, and the Mdr2
resultsMetabolomic profiling of LB-P8 cultures revealed increased detection of 10 metabolites involved in anti-fibrosis and anti-inflammation. RNA sequencing analysis of hepatic stellate cells showed downregulation of TGF-β, epithelial-mesenchymal transition (EMT,) and integrin signaling pathways. LB-P8 reduced liver fibrosis in BDL, DDC-fed, and Mdr2
conclusionsLB-P8 ameliorates cholestatic liver disease progression by reducing TGF-β-mediated fibroblast activation, and periportal accumulation of macrophages. Targeting the gut-liver axis with LB-P8 may represent a novel therapeutic strategy for PSC.
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