ArticleMedicine2026
Immune cells mediated the causal relationship between gut microbiota and carpal tunnel syndrome: A Mendelian randomization study.
Article in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Studies have shown that carpal tunnel syndrome (CTS) is associated with inflammation and immunity. Additionally, recent research indicates that the gut microbiota can influence the development and progression of immune and inflammatory responses. We aim to investigate the causal impact of gut microbiota on CTS and identify potential immune cell mediators. We made use of the summary statistics of 412 gut microbiota (from 7738 individuals), 731 immune cells (from 3757 individuals), and CTS (FinnGen consortium), from the extensive genome-wide association studies to date. To determine the causal links between gut microbiota and CTS, we employed bidirectional Mendelian randomization (MR) analyses, Bayesian-weighted Mendelian randomization (BWMR) and further employed 2-step MR to confirm potential mediating roles of immune cells. Moreover, we conducted rigorous sensitivity analyses to assess the heterogeneity, robustness, and horizontal pleiotropy of our findings. Bidirectional MR analysis and BWMR revealed that 15 bacterial traits were significantly associated with CTS, while the reversed causal relationship was not existed. Moreover, the mediation analysis demonstrated that 4 immune cells mediated the causal relationships of 3 gut microbiota species on CTS: CD14 on CD33dim HLA-DR+ CD11b+ cells and CD39 on CD39+ secreting CD4 regulatory T cells mediated the effects of s_Bacteroides_salyersiae on CTS, with indirect effect sizes of -0.0035 and -0.0015, accounting for 10.44% and 4.41% of the total effect, respectively. CD25 on IgD+ CD24+ B cells mediated the effect of s_Paraprevotella_clara on CTS, with an effect size of 0.0018, corresponding to 4.10% of the total effect. Moreover, CD8 on CD28+ CD45RA- CD8+ T cells mediated the association between s_Bacteroides_massiliensis and CTS, with a mediating effect of -0.0096, representing 10.49% of the total effect. The risk of CTS has been linked causally to gut microbiota, with 4 distinct immunophenotypes acting as potential mediators in this relationship. The role of gut microbiota in modulating immune cells, thereby influencing CTS, may offer novel therapeutic strategies and management approaches.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.