Gut Microbiota Modulation and Liver Injury Dynamics

Summary

The liver and gut microbiota are connected through a complex axis in which microbial communities influence hepatic health and resilience to injury. Modulation of gut bacteria can alter intestinal barrier function, systemic inflammation and metabolite profiles, thereby shaping the onset, progression and recovery of liver injury. Experimental models have demonstrated that specific bacterial strains or consortia can protect against chemical-induced hepatotoxicity by restoring epithelial integrity, suppressing pro-inflammatory cytokines and generating metabolites that inhibit regulated cell death pathways in hepatocytes. Conversely, gut dysbiosis exacerbates oxidative stress, promotes immune cell infiltration and heightens susceptibility to drug-induced or toxin-mediated liver damage. Recent advances in single-cell, multi-omics and transplantation approaches have illuminated key cellular actors in the gut-liver axis, identified novel therapeutic targets and provided the basis for microbiota-based interventions in acute and chronic liver diseases.

Research from Nature Portfolio

Recent studies have demonstrated that oral administration of selected Bifidobacterium strains before d-galactosamine exposure can substantially reduce acute liver injury in rodent models. In these experiments, Bifidobacterium pseudocatenulatum LI09 and Bifidobacterium catenulatum LI10 attenuated hepatocellular damage by reshaping gut communities, lowering bacterial translocation and dampening systemic cytokine surges. Improvements in ileal mucosal architecture and an increase in short-chain fatty acid producers correlated with reduced plasma M-CSF and chemokine levels, suggesting an immunomodulatory mechanism. In parallel, faecal microbiota transplantation into mice with d-galactosamine-induced acute liver failure restored key commensal taxa and rebalanced T-helper 17/regulatory T-cell cytokines, leading to marked amelioration of liver histopathology, transaminase elevations and pro-inflammatory mediators. These interventions underscore the capacity of whole-community or targeted probiotic approaches to re-establish homeostasis along the gut-liver axis.

Gut Microbiota Modulation and Liver Injury Dynamics publication trend

The graph below shows the total number of articles in gut microbiota modulation and liver injury dynamics across all publications each year (not limited to Nature Index journals).

Technical terms

Gut microbiota: The complex community of microorganisms residing in the gastrointestinal tract that influences host metabolism, immunity and barrier function.

Dysbiosis: An imbalance in the composition or function of the gut microbiota associated with disease states.

Hepatotoxicity: Liver damage caused by chemical compounds, drugs or toxins leading to elevated liver enzymes and tissue injury.

β-galactosidase: A microbial enzyme that cleaves lactose or related glycosides, enabling the release of bioactive compounds such as isoflavones.

Daidzein: A plant-derived isoflavone liberated by bacterial β-galactosidase, noted for its antioxidant and anti-ferroptotic properties in hepatocytes.

Ferroptosis: A regulated form of cell death driven by iron-dependent lipid peroxidation implicated in drug-induced liver injury.

Hypaphorine: A bacterial metabolite derived from Bifidobacterium species that modulates host circadian and oxidative stress pathways.

d-Galactosamine: A hepatotoxin used experimentally to induce acute liver failure by depleting nucleotide pools and provoking inflammatory responses.

References

  1. Liberation of daidzein by gut microbial β-galactosidase suppresses acetaminophen-induced hepatotoxicity in mice. Cell Host & Microbe (2023).
  2. Bifidobacterium adolescentis-derived hypaphorine alleviates acetaminophen hepatotoxicity by promoting hepatic Cry1 expression. Journal of Translational Medicine (2024).
  3. Bifidobacterium pseudocatenulatum LI09 and Bifidobacterium catenulatum LI10 attenuate D-galactosamine-induced liver injury by modifying the gut microbiota. Scientific Reports (2017).
  4. Fecal transplantation alleviates acute liver injury in mice through regulating Treg/Th17 cytokines balance. Scientific Reports (2021).

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