ArticleFrontiers in immunology2026
Multi-omics analysis identifies a hepatocyte-associated signature in alcohol-related liver injury.
Article in Frontiers in immunology, 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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Abstract
Alcohol-related liver disease (ALD) is a major cause of liver-related morbidity and mortality worldwide, yet the associations linking alcohol-induced gut microbial alterations to metabolic remodeling and hepatocyte dysfunction remain incompletely understood. Here, we applied an integrative multi-omics strategy combining untargeted fecal metabolomics, shotgun metagenomics, mouse liver bulk RNA sequencing, and reanalysis of publicly available human hepatic single-cell and bulk transcriptomic datasets to characterize alcohol exposure-associated gut-liver immunometabolic features. In a mouse model of acute ethanol-induced liver injury, fecal metabolomic and metagenomic profiling revealed marked alterations in microbial functional potential and fecal metabolic composition, identifying six convergent metabolic pathways across fecal multi-omics layers, including nucleotide metabolism, the pentose phosphate pathway, histidine metabolism, glycerophospholipid metabolism, glycine/serine/threonine metabolism, and the phosphotransferase system. Reanalysis of human ALD single-cell transcriptomes showed hepatocyte-enriched activity patterns for several corresponding pathways, suggesting potential pathway-level associations between fecal metabolic alterations and hepatic transcriptional responses. Integrative transcriptomic analysis further identified a ten-gene hepatocyte-associated signature, comprising LRG1, ORM1, ORM2, TAT, HP, FGB, FGG, ITIH3, NNMT, and AGT, which was associated with pathway activity and showed consistent upregulation across acute ethanol-induced liver injury and human ALD/AH transcriptomic datasets. In an external human cohort, this signature stratified patients into exploratory molecular subgroups with distinct metabolic pathway activities and clinical outcome distributions. Collectively, these findings provide a hypothesis-generating multi-omics framework for investigating alcohol-related liver injury and support further validation in chronic ethanol exposure models and functional studies.
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