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

Jan 27, 2026The American journal of Chinese medicine

Gut Microbes' Role in Immune and Nerve Interactions in Myasthenia Gravis: From Gut-Brain Links to New Treatments

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Abstract

Patients with myasthenia gravis (MG) exhibit reduced α-diversity and specific gut microbial signatures.

Distinct gut microbiota profiles in MG patients include depletion of beneficial bacteria and an increase in harmful microbes.
Lower levels of short-chain fatty acids (SCFAs) correlate with greater disease severity in MG.
Fecal microbiota transplantation (FMT) and probiotic treatment may improve MG symptoms by restoring immune balance and reducing inflammation.
Gut dysbiosis may worsen autoimmunity through activation of specific immune pathways and disruption of metabolic processes.
Further research is necessary to establish causal relationships and develop targeted microbiota-based therapies for MG.

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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 likeand, enrichment of pathobionts such asand, 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 likeameliorate 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. Bacteroides Bifidobacterium Escherichia Enterococcus Bifidobacterium

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

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