Elevated GABA and reduced secondary bile acids in Guillain-Barré syndrome: association with gut dysbiosis
In GBS patients, serum GABA was approximately 14.3-fold higher and multiple secondary bile acids were significantly reduced compared to healthy controls, alongside a distinct gut microbial pattern, but without causal evidence.
| Population | Patients with Guillain-Barré syndrome vs. healthy controls |
|---|---|
| Exposure | Untargeted serum metabolomics profiling and shotgun metagenomic sequencing of stool samples |
| Comparator | Healthy controls without GBS |
| Outcome | Serum GABA concentration; Serum secondary bile acids; Gut K. pneumoniae abundance; Gut Bacteroides sp. and Roseburia hominis abundance; Microbial genes in GABA biosynthesis pathway; Microbial genes in secondary bile acid pathways; Microbiota-metabolome correlation (Pearson) |
Summary of findings
| Outcome | Effect | 95% CI | Certainty | Clinical relevance | Notes |
|---|---|---|---|---|---|
| Serum GABA concentration | fold-change ~14.3 (GBS vs controls); 95% CI not reported | — | Low | — | 1 studies |
| Serum secondary bile acids | decreased in GBS vs controls (direction: lower); magnitude and 95% CI not reported | — | Low | — | 1 studies |
| Gut K. pneumoniae abundance | enriched in GBS vs controls; quantitative effect size and 95% CI not reported | — | Low | — | 1 studies |
| Gut Bacteroides sp. and Roseburia hominis abundance | decreased in GBS vs controls; quantitative effect size and 95% CI not reported | — | Low | — | 1 studies |
| Microbial genes in GABA biosynthesis pathway | enriched in GBS gut microbiome vs controls; quantitative effect size and 95% CI not reported | — | Low | — | 1 studies |
| Microbial genes in secondary bile acid pathways | decreased in GBS gut microbiome vs controls; quantitative effect size and 95% CI not reported | — | Low | — | 1 studies |
| Microbiota-metabolome correlation (Pearson) | Pearson r not reported with CI; associative only, in the causal inference | — | Low | — | 1 studies |
Context
GBS is a high-morbidity autoimmune polyneuropathy whose pathophysiology remains partially understood. The relationship between gut dysbiosis, serum metabolites, and aberrant immune responses in GBS lacks mechanistic human data. This study provides simultaneous metagenomics and metabolomics profiles in GBS patients, an approach still scarce in this condition.
What the study showed
Serum GABA was approximately 14.3-fold higher in GBS patients. Five secondary bile acids (methyl deoxycholate, glycodeoxycholic acid, glycolithocholic acid, taurolithocholic acid, and coprocholic acid) were significantly reduced. In the microbiota, Ligilactobacillus salivarius, Enterocloster bolteae, and Klebsiella pneumoniae were enriched, while Bacteroides sp., Roseburia hominis, and Paraprevotella xylaniphila were decreased. Prokaryotic genes in the GABA biosynthesis pathway were enriched in the gut microbiome; genes in secondary bile acid pathways were reduced.
How it was done
Cross-sectional observational study with simultaneous serum and stool collection from GBS patients and healthy controls. Untargeted metabolomics and shotgun metagenomics were applied. Multivariate analyses (PLS-DA) and Pearson correlation were used. Microbiological culture on seven different media was performed for pathogen isolation. Exact sample size and detailed demographic characteristics were not specified in the available text.
Effect magnitude
Serum GABA approximately 14.3-fold elevated in GBS vs. controls; formal 95% CIs and effect sizes (SMD, RR, OR) were not reported in the available text, limiting precise effect quantification.
Risk of bias
Cross-sectional design precludes causal inference. Sample size and population characteristics were not clearly described in the available abstract, preventing statistical power assessment. No adjustment for prior antibiotic use, diet, intravenous immunoglobulin, or plasmapheresis — all of which alter microbiota and metabolites. Pearson correlation does not establish causality. Formal risk-of-bias tools (e.g., ROBINS-I) were not applied or reported.
What this study does NOT prove
This study does not prove that gut dysbiosis causes GBS, nor that microbiota modulation alters disease course. Findings are associative and restricted to the studied population, not generalizable to other ethnicities, clinical GBS variants, or immunosuppressed patients.
In clinical practice
No direct therapeutic implication derives from this study. Clinicians should not modify clinical management based on these findings. The identification of K. pneumoniae in the GI tract of GBS patients warrants surveillance but not empirical treatment.
Limitations
Cross-sectional design precludes causal inference. Sample size and population characteristics were not clearly described in the available abstract, preventing statistical power assessment. No adjustment for prior antibiotic use, diet, intravenous immunoglobulin, or plasmapheresis — all of which alter microbiota and metabolites. Pearson correlation does not establish causality. Formal risk-of-bias tools (e.g., ROBINS-I) were not applied or reported.
What is still missing
Longitudinal studies with rigorous confounder control (antibiotics, diet, immunosuppression) and adequate sample size to determine whether microbial and metabolic alterations precede, accompany, or result from GBS.
Technical appendix
Version history
- 1.0 · 2026-06-27 — Auto-generated under Evidence Standard v1.0