ArticleFrontiers in immunology2024
The causality of gut microbiota on onset and progression of sepsis: a bi-directional Mendelian randomization analysis.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Gut microbiota-immune-metabolic crosstalk in acute lung injury: integrating the gut-lung axis from mechanism to therapeutic targeting.Seminars in immunopathology · 2026Review
- Engineered Lactate Catabolizing Probiotics Reveal Timescale Dependent Microbiome-Host Metabolic Coupling.bioRxiv : the preprint server for biology · 2026Article
- Narrative review on microbiota and sepsis: the host's betrayal?Internal and emergency medicine · 2026Review
- Gut microbiota dysbiosis in infants and young children with severe pneumonia and sepsis: a matched case-control study identifying potential biomarkers for early risk stratification.Frontiers in immunology · 2026Article
- Causal effect of gut microbiota on venous thromboembolism: a two-sample mendelian randomization study.Thrombosis journal · 2024Article
- Causal Effects of Sleep Quality on Primary Headache and the Mediation via Gut Microbiota: A Mendelian Randomization Study.Brain and behavior · 2024Article
- Genetically Predicted Peripheral Immune Cells Mediate the Effect of Gut Microbiota on Influenza Susceptibility.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
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Abstract
Background: Several observational studies have proposed a potential link between gut microbiota and the onset and progression of sepsis. Nevertheless, the causality of gut microbiota and sepsis remains debatable and warrants more comprehensive exploration. Methods: We conducted a two-sample Mendelian randomization (MR) analysis to test the causality between gut microbiota and the onset and progression of sepsis. The genome-wide association study (GWAS) summary statistics for 196 bacterial traits were extracted from the MiBioGen consortium, whereas the GWAS summary statistics for sepsis and sepsis-related outcomes came from the UK Biobank. The inverse-variance weighted (IVW) approach was the primary method used to examine the causal association. To complement the IVW method, we utilized four additional MR methods. We performed a series of sensitivity analyses to examine the robustness of the causal estimates. Results: We assessed the causality of 196 bacterial traits on sepsis and sepsis-related outcomes. Genus Conclusion: This MR analysis unveiled a causality between the 21 bacterial traits and sepsis and sepsis-related outcomes. Our findings may help the development of novel microbiota-based therapeutics to decrease the morbidity and mortality of sepsis.
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