ArticleJournal of inflammation research2025
Using Olink Proteomics to Identify Inflammatory Biomarkers in the Cerebrospinal Fluid in Guillain-Barré Syndrome.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Immunological, Inflammatory, and Microbiota Determinants of Carpal Tunnel Syndrome: Evidence from Mendelian Randomization.Endocrine, metabolic & immune disorders drug targets · 2026Article
- MCC950 Alleviates Experimental Autoimmune Neuritis by Inhibiting NLRP3 Inflammasome Activity and Down-Regulating Interleukin-23/Interleukin-17 Axis Expression.Journal of inflammation research · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: The precise etiology of Guillain-Barré syndrome (GBS) is uncertain; however, it is linked to immunological and inflammatory processes. Thus, this research aims to investigate new inflammatory biomarkers for GBS diagnosis. Patients and Methods: In this work, Olink proteomics was used to compare the expression levels of 92 inflammation-related proteins in the cerebrospinal fluid (CSF) of patients with non-inflammatory neurological diseases (n=14) and GBS (n=23). Differentially expressed proteins (DEPs) were then analyzed biologically and in terms of their relationship to clinical features, and logistic regression models were built. We also downloaded GEO data to validate DEPs at the mRNA level. Results: We identified twenty DEPs. The PPI network screened six key DEPs (including TNF, CCL20, IL8, MCP-1, IL10, and IL5). These DEPs were enriched in the chemokine signaling pathway, the IL-17 signaling pathway, cytokines and their receptor interactions, and other pathways. TNFRSF9 and IL-10RB showed the strongest correlation of expression in CSF. CCL20 and IL5 could be used as potential independent predictors for the diagnosis of GBS. Seven DEPs (MCP-1, CXCL1, MCP-4, MMP-10, CXCL10, CCL28, and CCL20) had some predictive value for the severity of GBS. Based on the validation of the GEO data, the mRNA expression of MCP-1 and CXCL9 was found to be upregulated at the peak of EAN, and the enriched pathways at the gene transcription level were consistent with the results of this study. Conclusion: DEPs linked to inflammation (such as TNF, CCL20, IL8, MCP-1, IL10, and IL5) could be useful biomarkers for GBS diagnosis. More research is required to determine their precise mechanisms in GBS.
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.