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Article Abstract
Background: Interactions between immune phenotypes and metabolites in sepsis pathogenesis remain poorly defined. We integrated Mendelian randomization (MR) and single-cell transcriptomics to investigate metabolic mediation in immune-sepsis associations.
Methods: Bidirectional two-sample MR analyzed sepsis GWAS (11,643 cases), 1,400 metabolites, and 731 immune phenotypes. Single-cell analysis of GSE167363 (sepsis vs. controls) included clustering, differential expression, and pathway enrichment.
Results: CD39 expression was upregulated in sepsis immune cells. MR identified CD3 + CD39 + CD8+ T cells as risk factors for sepsis incidence (OR = 1.053, P = 0.008) and 28-day mortality (OR = 1.108, P = 0.037). These cells correlated with 73 metabolites, notably androsterone sulfate, which mediated 4.97% of sepsis risk (P = 0.026).
Conclusion: CD39 + CD8+ T cells drive sepsis progression through metabolic intermediates like androsterone sulfate, highlighting immunometabolic crosstalk as a therapeutic target.
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