Frontiers in microbiology · 2026
From probiotic depletion to inflammatory cascade: multi-omics reveals the temporal progression of sleep deprivation-induced gut-liver axis disruption in mice.
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Dai Ming-Kun, Kuang Xiao, Wang Yi-Fei, Liu Xiao-Xiao, Jin Yong-Fan, Li Yi-Ying, Tai Wen-Lin
Аннотация
INTRODUCTION: Sleep deprivation (SD) is increasingly recognized as a risk factor for metabolic and hepatic disorders, yet the temporal dynamics linking gut dysbiosis to liver injury remain poorly characterized.
METHODS: In this study, we established a platform-based SD model in a total of 24 C57BL/6J mice (n = 4 per group per weekly time point) over 3 weeks and systematically investigated the weekly progression of gut microbiome alterations, hepatic metabolite profiles, and liver injury markers using Accu16S® absolute quantification sequencing and untargeted LC-MS/MS metabolomics.
RESULTS: Our results revealed a temporally ordered three-stage cascade of gut-liver axis disruption. In week 1, core probiotics including Bifidobacterium and Dubosiella declined concurrently with protective metabolites such as tryptamine and glycocholic acid, alongside perturbation of primary bile acid biosynthesis. In week 2, concurrent enrichment of a compensatory Lactobacillaceae member (Ligilactobacillus) and an opportunistic pathogen (Streptococcus) was accompanied by reduced microbiota-metabolite correlation density, coinciding with peak serum ALT/AST levels and metabolic pathway remodeling involving nucleotide sugar and tryptophan metabolism. By week 3, synchronous decline of Lactobacillus, Bifidobacterium, and Dubosiella coincided with full-scale activation of arachidonic acid metabolism and inflammatory immune pathways, accompanied by elevated serum LPS levels suggestive of intestinal barrier perturbation. Correlation analyses revealed that the progressive depletion of beneficial bacteria was associated with the sequential loss of protective metabolites, reorganization of the metabolic network, and inflammatory mediator accumulation, although these relationships remain correlational and require causal validation.
DISCUSSION: These findings describe a "protective loss-homeostatic decoupling-inflammatory signature" descriptive model. Because these findings are based on correlation analyses in a mouse model without causal validation, further mechanistic and interventional studies are required before any clinical implications can be drawn.
METHODS: In this study, we established a platform-based SD model in a total of 24 C57BL/6J mice (n = 4 per group per weekly time point) over 3 weeks and systematically investigated the weekly progression of gut microbiome alterations, hepatic metabolite profiles, and liver injury markers using Accu16S® absolute quantification sequencing and untargeted LC-MS/MS metabolomics.
RESULTS: Our results revealed a temporally ordered three-stage cascade of gut-liver axis disruption. In week 1, core probiotics including Bifidobacterium and Dubosiella declined concurrently with protective metabolites such as tryptamine and glycocholic acid, alongside perturbation of primary bile acid biosynthesis. In week 2, concurrent enrichment of a compensatory Lactobacillaceae member (Ligilactobacillus) and an opportunistic pathogen (Streptococcus) was accompanied by reduced microbiota-metabolite correlation density, coinciding with peak serum ALT/AST levels and metabolic pathway remodeling involving nucleotide sugar and tryptophan metabolism. By week 3, synchronous decline of Lactobacillus, Bifidobacterium, and Dubosiella coincided with full-scale activation of arachidonic acid metabolism and inflammatory immune pathways, accompanied by elevated serum LPS levels suggestive of intestinal barrier perturbation. Correlation analyses revealed that the progressive depletion of beneficial bacteria was associated with the sequential loss of protective metabolites, reorganization of the metabolic network, and inflammatory mediator accumulation, although these relationships remain correlational and require causal validation.
DISCUSSION: These findings describe a "protective loss-homeostatic decoupling-inflammatory signature" descriptive model. Because these findings are based on correlation analyses in a mouse model without causal validation, further mechanistic and interventional studies are required before any clinical implications can be drawn.