ArticleGut pathogens2025
Comparative study of liver injury protection by Akkermansia muciniphila and Faecalibacterium prausnitzii interventions in live and cell-free supernatant forms via targeting the hepcidin - ferroportin axis in mice with CCl₄-induced liver fibrosis.
Article in Gut pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Preventive and therapeutic effects of co-administration of Bacteroides thetaiotaomicron and infliximab on dextran sodium sulfate-induced colitis in mice.Intestinal research · 2026Article
- Barrier-Immune Gating Failure in Gut-Brain Neuroinflammation: A Working Hypothesis and Conceptual Framework.Behavioural neurology · 2026Review
- Mechanism and application ofFrontiers in cellular and infection microbiology · 2026Review
- Adipose-derived stem cell extracellular vesicles attenuate liver fibrosis via restoration of gut barrier function and modulation of gut microbiota.Extracellular vesicles and circulating nucleic acids · 2025Article
- Collecting the evidence: mechanistic insights intoFrontiers in immunology · 2025Review
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10 authors.
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Abstract
backgroundliver fibrosis is associated with dysregulated iron homeostasis regulated by the hepcidin-ferroportin axis, and dysbiotic gut microbiota. This study aimed to investigate the preventive and ameliorative effects of live and cell-free supernatant (CFS) forms of Akkermansia muciniphila and Faecalibacterium prausnitzii, as important gut microbiota members, on liver fibrosis by targeting the hepcidin-ferroportin axis in both in vitro and in vivo models.
methodsAt the in vitro level, the effects of A. muciniphila and F. prausnitzii on the expression of collagen type I alpha 1 (COL1A1) and ferroportin (SLC40A1) transcripts in hepatic stellate cells (HSCs) were evaluated in transforming growth factor beta (TGFβ)-activated LX-2 cells, a human hepatic stellate cell line. In vivo, male C57BL/6 mice were intraperitoneally (IP) injected with 10% carbon tetrachloride (CCl₄) twice weekly for 6 weeks to establish the liver fibrosis model. Administration of live and CFS forms of A. muciniphila and F. prausnitzii was initiated 10 days before CCl₄ injection and continued until the end of the experiment. Liver injury and fibrosis were assessed using serum markers, hematoxylin and eosin (H&E), and Masson's trichrome staining. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC) were used to evaluate the effects of the interventions on gene expression related to the hepcidin-ferroportin axis in liver, colon and brain samples. Additionally, qPCR was used to determine alterations in the relative abundance of key gut microbiota members in fecal samples.
resultsBoth A. muciniphila and F. prausnitzii, as well as their CFS, significantly downregulated COL1A1 expression in TGFβ-activated LX-2 cells, accompanied by reduced alpha-smooth muscle actin (α-SMA) protein expression in liver tissue. In vivo, intervention with F. prausnitzii, particularly its CFS, led to a greater induction of hepatic hepcidin and ferroportin expression compared to A. muciniphila and its CFS. Serum liver injury markers (alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH)) and iron levels were markedly improved following treatment with live F. prausnitzii and its CFS. Additionally, F. prausnitzii CFS significantly enhanced hepcidin gene expression in brain tissue, suggesting broader systemic benefits.
conclusionWe demonstrated that F. prausnitzii and its CFS had greater beneficial potential than A. muciniphila and its CFS in the prevention and amelioration of liver fibrosis, likely through modulation of the hepcidin-ferroportin axis. These findings may support the development of next-generation probiotics and postbiotics for liver injury, which warrants further investigation.
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