ArticleClinical & translational immunology2026
Gut metabolites identified in cerebrospinal fluid of genetic interferonopathy support gut-brain endothelial dysfunction.
Article in Clinical & translational immunology, 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Aicardi-Goutières syndrome (AGS) is a rare genetic interferonopathy because of aberrant DNA or RNA metabolism with secondary host anti-viral (interferon) activation. This metabolomics study aimed to improve the biological understanding of AGS and explore potential biomarkers. Methods: We performed untargeted cerebrospinal fluid (CSF) metabolomics using a UPLC-Q-Exactive-HFx Mass Spectrometry of 10 genetically confirmed AGS patients (8 males, mean 4.8 years, range 0.2-16.5) and age-sex matched controls. Metabolites were then quantified and validated using UHPLC-QqQ-MS/MS in CSF and serum. Results: We identified expected elevated inflammatory metabolites (neopterin and kynurenine) and unexpected elevated gut microbe metabolites in CSF samples: Indole, p-Cresol, γ-Butyrobetaine and N-Butyryl-L-homoserine lactone (all Conclusion: Our findings suggest gut microbe metabolite leakage traversing the gut-blood-brain barrier in AGS, potentially because of endothelial dysfunction.
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.