Evidence map›Paper›PMID 42100652›Full record

ArticleFrontiers in cellular and infection microbiology2026

Functional metagenomic reconstruction of microbial pathways altered by probiotic supplementation in liver failure.

Junli Luo, Yuhan Feng, Jinzi Chen, Nuo Xu, Guoqin Zhang, Jiawei Ni, Cai Li

Abstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Junli LuoDepartment of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yuhan FengDepartment of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jinzi ChenDepartment of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Nuo XuDepartment of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Guoqin ZhangDepartment of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jiawei NiDepartment of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Cai LiDepartment of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Liver failure is a severe condition marked by circulatory failure, systemic inflammation, and gut microbial dysbiosis. This dysbiosis worsens liver damage by reducing beneficial metabolites and increasing harmful products. This study investigates the effects of probiotics on gut microbial functional pathways in liver failure. The aim is to link microbial metabolic reprogramming with host biochemical, inflammatory, and gut barrier responses through functional metagenomic reconstruction. Methods: Acute liver failure was induced in male Wistar rats using D-galactosamine (700 mg/kg) and lipopolysaccharide (10 μg/kg). Probiotic treatment began 24 hours after induction and was administered daily for 14 consecutive days before euthanasia. Two doses were used: low (1×10⁸ CFU/day) and high (1×10⁹ CFU/day). Fecal samples underwent shotgun metagenomic sequencing, followed by functional pathway reconstruction. These predictions were validated using metabolite profiling, quantitative PCR of microbial genes, intestinal barrier assays, and immune cell cytokine analysis. Host phenotypic markers were correlated with microbial pathways. Results and discussion: Liver failure significantly elevated serum ALT (42.6±6.8 to 512.4±48.9 U/L), AST (78.3±9.5 to 684.7±62.1 U/L), and plasma ammonia (38.9±5.2 to 128.6±14.3 μmol/L). Probiotic supplementation showed a dose-dependent improvement. ALT dropped to 382.7±41.6 U/L (low dose) and 248.9±32.4 U/L (high dose). Ammonia levels decreased to 86.4±9.7 μmol/L and 59.8±7.6 μmol/L, respectively. Metagenomic analysis revealed a 1.7- and 2.6-fold increase in short-chain fatty acid (SCFA) biosynthesis pathways and a 38% and 61% decrease in urease-associated nitrogen metabolism. These changes were confirmed by higher fecal SCFAs (31.8±4.2 to 63.9±6.4 mM), lower ammonia (8.9±1.1 to 3.7±0.5 mM), improved intestinal barrier integrity (TEER: 462±38 to 721±44 Ω·cm²), and reduced TNF-α (214.6±22.8 to 74.9±12.3 pg/mL). Probiotic supplementation significantly reprogrammed the gut microbiome in liver failure. This highlights its potential as a therapeutic modulator of the gut-liver axis.

Indexed as

Gastrointestinal MicrobiomeLiver FailureLiver Failure, AcuteMetagenomicsProbioticsAmmoniaAnimalsCytokinesDisease Models, AnimalFecesGalactosamineIntestinal Barrier FunctionMaleRatsRats, WistarAmmoniaCytokinesGalactosamineammonia metabolismfunctional metagenomicsgut–liver axisliver failureprobioticsshort-chain fatty acids

Identifiers

PMID42100652
PMCPMC13144039

What Socratic holds

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LicenceCC BY
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.