This review examines the bidirectional relationship between the gut microbiome and multiple sclerosis (MS). Analyzing current literature from PubMed and Google Scholar, the paper confirms that MS patients consistently display gut dysbiosis. This is characterized by reduced microbial diversity, a depletion of anti-inflammatory, short-chain fatty acid-producing bacteria, and an overabundance of pro-inflammatory taxa. This imbalance contributes to intestinal barrier dysfunction ("leaky gut"), systemic inflammation, and the activation of neurotoxic T cells, which exacerbates neuroinflammation. Notably, the interaction is reciprocal; common disease-modifying therapies also influence gut microbiota composition. The review concludes that these complex interactions present new opportunities for adjunctive therapies. Emerging evidence supports the potential of microbiome-targeted strategies, including probiotics, prebiotics, dietary changes, and butyrate supplementation, to reduce inflammation and alleviate symptoms, paving the way for more personalized MS management. Introduction: Multiple sclerosis (MS) is a chronic, immune-mediated disorder of the central nervous system and a leading cause of neurological disability in young adults. Its pathogenesis involves a complex interplay between genetic susceptibility and modifiable environmental factors. In recent years, the gut microbiota has emerged as a critical regulator of systemic immunity and a potential key modulator of neuroinflammation via the microbiota-gut-brain axis. Purpose of the work: This review aims to synthesize current evidence on the bidirectional relationship between gut microbiota and multiple sclerosis. It focuses on the molecular mechanisms linking dysbiosis to neuroinflammation, the clinical impact of microbiota alterations in MS patients, and the therapeutic potential of microbiome-targeted interventions. Materials and methods: A comprehensive analysis of scientific articles available on PubMed and Google Scholar was conducted. The search strategy included combinations of keywords such as "multiple sclerosis", "gut microbiota", "dysbiosis", "short-chain fatty acids", "microbiota-gut-brain axis", "immunomodulation", and "probiotics". Studies published in peer-reviewed journals, including original research, meta-analyses, and clinical trials, were selected for review. Results: The review confirms that MS patients exhibit significant gut dysbiosis characterized by reduced microbial diversity, depletion of short-chain fatty acid (SCFA)-producing bacteria (e.g., Faecalibacterium, Butyricicoccus), and an increase in pro-inflammatory taxa (e.g., Prevotella). This dysbiosis contributes to increased intestinal permeability ("leaky gut"), systemic low-grade inflammation, and activation of encephalitogenic T cells (Th1/Th17), which exacerbate neuroinflammation and demyelination. Clinical data indicate that over 75% of MS patients report gastrointestinal symptoms, correlating with microbiota alterations. Importantly, the review highlights that standard disease-modifying therapies (e.g., interferon-beta, dimethyl fumarate, ocrelizumab) can themselves modulate gut microbiota composition, suggesting a bidirectional drug-microbiome interaction. Furthermore, emerging evidence supports the therapeutic potential of microbiota-targeted strategies: probiotic supplementation (Lactobacillus, Bifidobacterium) reduces inflammatory markers and improves disability scores; prebiotic fibers (e.g., inulin) enhance SCFA production and attenuate experimental autoimmune encephalomyelitis; dietary interventions alleviate fatigue and improve quality of life; and butyrate, a key SCFA, promotes remyelination. Fecal microbiota transplantation has shown promise in achieving long-term disease stabilization in isolated cases.
Jętasiewicz et al. (Mon,) studied this question.