ArticleFrontiers in immunology2024
Causal relationships between gut microbiota, immune cell, and Henoch-Schönlein Purpura: a two-step, two-sample Mendelian randomization study.
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 5 papers.
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Who cites it
5 citing papers in PubMed.
- Clinical efficacy and gut microbiota profiling by 16S rRNA sequencing in children with Henoch-Schönlein purpura treated with integrated Chinese and Western medicine.Frontiers in microbiology · 2026Article
- Gut microbiota in Henoch-Schönlein purpura: from pathogenesis to therapeutic strategies.Frontiers in immunology · 2026Review
- Unraveling the gut-immune-kidney axis in kidney stone disease: a two-step Mendelian randomization investigation.Urolithiasis · 2025Article
- The causal relationships between inflammatory cytokines, blood metabolites, and thyroid cancer: a two-step Mendelian randomization analysis.Discover oncology · 2025Article
- Epigastric pain of unknown origin, esophageal and gastric involvement: a Henoch-Schönlein Purpura case report.Frontiers in medicine · 2025Article
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Authors and funding
8 authors.
Funding
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Abstract
Background: Regulating the immune system is a crucial measure of gut microbiota (GM) that influences the development of diseases. The causal role of GM on Henoch-Schönlein Purpura (HSP) and whether it can be mediated by immune cells is still unknown. Methods: We performed a two-sample Mendelian randomization study using an inverse variance weighted (IVW) method to examine the causal role of GM on HSP and the mediation effect of immune cells between the association of GM and HSP. Results: We demonstrated the causal relationships between 14 axas and 6 pathways with HSP. Additionally, we identified 9 immune cell characteristics associated with HSP. Importantly, through mediation MR analysis, we identified several immune cell characteristics that mediate the impact of GM on HSP. For instance, Genus_Blautia affects HSP via Monocyte (HLA DR on CD14+ CD16- monocyte) and Monocyte (HLA DR on monocyte). The proportion of mediation effects further elucidated the complex dynamics between GM exposure, immune markers, and their combined impact on HSP. Conclusion: The study suggested a causal relationship between GM and HSP, which may be mediated by immune cells.
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