ArticleScientific reports2025
Gut dysbiosis in multiple sclerosis patients: a comparative analysis in fecal samples.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Association between Mediterranean Diet and Development of Multiple Sclerosis: A Systematic Review and Meta-Analysis.Brain and behavior · 2026Pooled it
- Bifidobacteria: biogeography, host adaptation and ecological functions.Nature reviews. Microbiology · 2026Review
- The Microbiome-Neurodegeneration Interface: Mechanisms, Evidence, and Future Directions.Cells · 2026Review
- Gut microbiota and brain aging: a comparative review of African and western populations.Frontiers in aging neuroscience · 2026Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a chronic, inflammatory disease of the central nervous system characterized by neuroinflammation, demyelination, and axonal damage. Recent evidence suggests that gut microbiota may play a critical role in MS pathogenesis by modulating immune responses and contributing to systemic inflammation. Alterations in the abundance of specific bacterial species, such as Bacteroides fragilis, Faecalibacterium prausnitzii, and Bifidobacterium spp., have been linked to immune dysregulation in MS. However, the role of gut microbiota in treatment-naïve patients at the earliest stages of MS remains underexplored. This case-control study, conducted from 2021 to 2023, included 36 treatment-naïve patients with MS (PwMS) who had experienced their first attack of symptoms and fulfilled McDonald's criteria, and 36 age- and sex-matched healthy controls. Stool samples were collected and analyzed using quantitative PCR (qPCR) to determine the relative abundance of Bacteroides fragilis, Faecalibacterium prausnitzii, and Bifidobacterium spp.. Statistical analyses compared bacterial abundance between groups while controlling for key demographic variables. The MS group included 9 males (25%) and 27 females (75%), with a mean age of 38.3 ± 9.5 years, compared to 39.8 ± 10.2 years in controls. PwMS exhibited significantly lower levels of Bacteroides fragilis (0.11 × 10⁹ vs. 0.22 × 10⁹ CFU, p < 0.05) and Bifidobacterium spp. (1.50 × 10⁹ vs. 1.65 × 10⁹ CFU, p < 0.05) compared to controls. Although Faecalibacterium prausnitzii levels were lower in PwMS (1.08 × 10⁹ vs. 1.27 × 10⁹ CFU), the difference was not statistically significant. These findings align with emerging evidence suggesting a potential role of gut dysbiosis in MS pathogenesis. The reduced abundance of beneficial bacteria, particularly B. fragilis and Bifidobacterium spp., may contribute to altered immune regulation and increased inflammation in PwMS. While these results contribute to our understanding of the gut-brain axis in MS and may inform future therapeutic approaches, further research, including larger longitudinal studies, is needed to clarify the complex relationship between gut microbiota and MS development and progression.
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