ArticleFASEB bioAdvances2025
Circulating Inflammatory Proteins Mediate the Causal Effect of Gut Microbiota on Inflammatory Bowel Disease: Bayesian and Mediated Mendelian Randomization.
Article in FASEB bioAdvances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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Authors and funding
3 authors.
Funding
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Abstract
Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), presents a global public health challenge. Although the relationships between gut microbiota, inflammatory proteins, and IBD are recognized, their causal associations and mediating roles remain unclear. Large-scale genome-wide association study data on 473 gut microbiota, 91 circulating inflammatory proteins, and IBD (including CD and UC) were analyzed. Univariable Mendelian randomization (UVMR), Bayesian Weighted MR (BWMR), mediation MR, and sensitivity analyses were used to explore causal associations and quantify mediating effects. MR results indicate that 24, 20, and 22 gut microbiota exhibit causal effects on IBD (nine protective factors, 15 risk factors), CD (nine protective factors, 11 risk factors) and UC (seven protective factors, 15 risk factors). Three inflammatory proteins (one protective factors, two risk factors) have causal effects on IBD, with five having causal effects on CD (one protective factors, four risk factors) and UC (two protective factors, three risk factors). Mediation analysis reveals that Interleukin-17C levels mediate the causal effects of
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