ArticleFrontiers in immunology2026
Inflammatory protein mediators linking gut microbiota to degenerative lumbar spine disorders: cross-disease genetic evidence.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Degenerative lumbar spine disorders (DLSD), including intervertebral disc disorders (IDD), degenerative spondylolisthesis, and lumbar spinal stenosis (LSS), are major contributors to low back pain and disability. Associations among gut microbiota (GM), inflammatory proteins, and DLSD have been demonstrated in prior studies. Yet, two key questions persist: whether specific circulating inflammatory proteins (IPs) mediate this association, and whether such mediation is shared across different diseases. Methods: We performed two-sample Mendelian randomization (MR) to evaluate causal associations among 473 GM taxa, 91 circulating IPs, and three DLSD outcomes using FinnGen R12 summary statistics. Causal estimates were obtained using inverse-variance weighted MR with complementary sensitivity analyses, pleiotropy and heterogeneity testing, and bidirectional MR. Two-step MR mediation was applied to quantify indirect effects of GM through IPs. Experimental validation was performed using rat models, with qPCR and ELISA assessing inflammatory markers in lumbar tissues and metagenomic sequencing evaluating gut microbiota profiles. Results: Genetically predicted GM taxa were associated with LSS (28 taxa), spondylolisthesis (20 taxa), and IDD (41 taxa). IP MR identified risk-increasing associations for LSS (4E-BP1 and interleukin-4), spondylolisthesis (CXCL1, CXCL5, FGF-5, IL-15RA, and IL-4) and IDD (IL-20RA and IL-6), while IL-18 showed a protective association with IDD that remained robust after multiple-testing correction. Mediation analyses identified 13 genetically supported putative GM-IPs-DLSD pathways, highlighting convergent mediators including PD-L1 for spondylolisthesis and IL-6 and IL-18 for IDD, with mediation proportions ranging from 7.55% to 13.22% across key pathways. Experimental results showed inflammatory activation and gut microbiota alterations in disease models, with partial concordance with the MR findings. Conclusions: These findings support a genetically determined microbiota-inflammation axis in DLSD. Furthermore, they identify circulating inflammatory proteins as mediators to prioritize mechanistic studies and guide translational follow-up research.
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.