Causal relationships between new 412 gut microbiota, 731 inflammatory cells,91 inflammatory proteins and circulating leukocytes and subarachnoid hemorrhage: a Multi-omics, Bidirectional Mendelian randomization study and Meta-analysis

Abstract

Abstract Background A neurological emergency with potentially fatal outcomes is subarachnoid hemorrhage (SAH). Arachnoid and soft meninges are separated by a tiny gap called the subarachnoid space. The term "SAH" describes a clinical state brought on by bleeding into the subarachnoid space as a result of diseased or damaged blood vessels rupturing at the base or surface of the brain. Methods To obtain preliminary results, this study integrated the use of several omics with Mendelian randomization analysis and MR-IVW, MR Egger, MR weight median, and MR weight mode. Reverse Mendelian randomization analysis using subarachnoid hemorrhage as exposure. Lastly, to get a summary of the findings, conduct a meta-analysis on the preliminary data. Results GBPA-Pyridoxal 5 photosphate biosynthatis I (OR = 1.48,95% CI, 1.04–2.12) and GBPA-glucose biosynthesis I(OR = 0.68,95% CI, 0.52–0.90)is positively correlated with SAH. The urokinase type plasma activator levels showed a positive correlation with SAH (OR = 1.17,95% CI, 1.04–1.32).CD80 on CD62L + Plasmacytoid Dendritic Cell, CD80 on plasmacytoid Dendritic Cell, CD123 on CD62L + plasmacytoid Dendritic Cell and SSC-A on Plasmacytoid Dendritic Cell were found to be associated with SAH. Conclusion Using Mendelian randomization and meta-analysis, four inflammatory cells, one inflammatory protein, and two new gut microbiota-related pathways were shown to be connected to SAH in this investigation. suggesting that each of these could be a potential treatment target for SAH. This implies that controlling gut microbiota and using anti-inflammatory medications are essential for treating SAH.