Volume 29, Issue 163, September 2025

The Role of Gut Microbiota in Multiple Sclerosis: Mechanisms and Therapeutic Potential

Jan Wojdal^1♦, Katarzyna Ciepłucha², Aleksandra Wądołowska³, Barbara Przybył⁴, Zuzanna Mogilany⁵, Blanka Serafin-Juszczak⁶, Karolina Kusek⁷, Maria Wydra⁸, Michał Wilk⁹, Daniel Narożniak¹⁰

¹Copernicus Memorial Hospital, Pabianicka 62, 93-513, Łódź, Poland
²Rydygier Specialist Hospital in Krakow, Osiedle Złotej Jesieni 1, 31- 820 Kraków, Poland
³University Clinical Hospital No. 1 of the Medical University of Lodz, Kopcińskiego 22, 90-153 Łódź, Poland
⁴University Clinical Hospital No. 2 of the Medical University of Lodz; Stefana Żeromskiego 113, 90-549 Łódź, Poland
⁵Hospital of the Ministry of Interior and Administration in Lodz, Północna 42, 91–425 Łódź: Lodz, Poland
⁶University Clinical Hospital No. 2 of the Medical University of Lodz: Łódź, ul. Stefana Żeromskiego 113, 90-549 Łódź, Poland
⁷Central Clinical Hospital of Medical University of Lodz; Pomorska 251, 92-213 Łódź, Poland
⁸Rydygier Specialist Hospital in Krakow; Osiedle Złotej Jesieni 1, 31- 820 Kraków, Poland
⁹Central Clinical Hospital, of Medical University of Lodz; Pomorska 251, Łódź, Poland
¹⁰St. Raphael’s Voivodeship Specialist Hospital in Czerwona Góra, Czerwona Góra 10, 26-060 Chęciny, Poland

^♦Corresponding author
Jan Wojdal, Copernicus Memorial Hospital, Pabianicka 62, 93-513, Łódź, Poland

ABSTRACT

Background: Dysbiosis of the gut microbiota is a modifiable factor in multiple sclerosis pathology, but its clinical significance and therapeutic potential are still uncertain. Aim: Summarise current evidence on (i) characteristic gut microbiota changes in MS, (ii) mechanistic links between dysbiosis and neuro-immune injury, and (iii) early outcomes of microbiota-targeted interventions. Methods: PubMed, Scopus, and Google Scholar were searched (January 2010 – April 2025) using the terms: multiple sclerosis, gut microbiota, dysbiosis, short-chain fatty acids, and faecal microbiota transplantation. We included original human and animal studies, clinical trials, and reviews. During this research, 108 records were analysed narratively. Results: Key findings indicate that MS involves a reduction in shortchain fatty acid (SCFA) producers such as Faecalibacterium, Roseburia, and Prevotella, and an increase in mucin-degraders, including Akkermansia, Methanobrevibacter, and Ruminococcus gnavus. Notably, a Blautia: Akkermansia ratio ≤ 0.5, low faecal butyrate/propionate, and high serum zonulin or LPS-binding protein are associated with higher relapse risk and grey-matter loss. The evidence suggests dysbiosis amplifies Th17 cell immunity, weakens Treg control, increases endotoxemia, and activates astrocytes. Interventions such as fibre-rich or Mediterranean diets, oral propionate, certain probiotics, and faecal microbiota transplantation have been shown to normalise SCFAs and Th17:Treg ratios, resulting in early reductions in relapse rate and brain atrophy. Conclusions: Gut dysbiosis is a disease-modifying factor in MS. Strategies based on diet, metabolites, or barrier-protective microbiota should be tested in larger, placebo-controlled trials alongside standard disease-modifying therapies.

Keywords: Multiple sclerosis; Gut microbiota; Dysbiosis; Short-chain fatty acids; Propionate; Th17/Treg balance; Faecal microbiota transplantation; Probiotics

Medical Science, 2025, 29, e168ms3714

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DOI: https://doi.org/10.54905/disssi.v29i163.e168ms3714

Published: 18 September 2025