Gut Microbiota as Neuroimmune Modulators in Myasthenia Gravis: Mechanistic Insights from the Gut-Brain Axis to Therapeutic Innovations

Myasthenia gravis (MG) is a chronic autoimmune disorder characterized by an immune-mediated attack on neuromuscular junction acetylcholine receptors (AChRs), and its pathogenesis is closely linked to immune dysregulation. Emerging evidence has highlighted the pivotal role of the gut microbiota in the pathophysiology of MG through immunomodulation, microbial metabolite signaling, and gut-brain axis interactions. This review combines 16S rRNA sequencing, metagenomic, and metabolomic data to reveal distinct gut microbial signatures in patients with MG. These signatures include reduced α-diversity, depletion of beneficial taxa like Bacteroides and Bifidobacterium, enrichment of pathobionts such as Escherichia and Enterococcus, and diminished levels of the short-chain fatty acids (SCFA), which were inversely correlated with disease severity. Experimental models have demonstrated that fecal microbiota transplantation (FMT) and probiotic supplementation with strains like Bifidobacterium ameliorate symptoms by restoring Th17/Treg equilibrium, suppressing the expression of pro-inflammatory cytokines including IL-6 and TNF-α, and enhancing intestinal barrier integrity. Mechanistically, gut dysbiosis exacerbates autoimmunity via NF-αB pathway activation, disrupts tryptophan metabolism and impairs gut-brain signaling. While existing studies have established microbiota-MG associations, further causal validation, personalized therapeutic strategies, and multi-omics integration remain critical priorities. Microbiota-targeted interventions, including precision FMT and metabolite delivery, hold translational potential, but their validation via large-scale randomized controlled trials and interdisciplinary approaches like AI-driven microbiota profiling is essential if they are to advance precision medicine for MG management.