ArticleFrontiers in cellular and infection microbiology2026
Disruption of intestinal barrier and immune homeostasis links gut microbiota dysbiosis to aggravated experimental autoimmune myasthenia gravis.
Article in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Abstract
Introduction: Myasthenia Gravis (MG) is an acquired autoimmune disease. The imbalance between Th17 and Treg cells plays a crucial role in the pathogenesis of MG. A stable intestinal microbiota is essential for maintaining immune balance, a function primarily mediated by the Th17/Treg axis. This study aims to explore the role of gut microbiota in the pathogenesis of experimental autoimmune myasthenia gravis (EAMG) to identify potential new treatment strategies. Methods: An EAMG model was established in Lewis rats by immunization with the AChRα97-116 peptide segment. The composition and structure of the gut microbiota were analyzed by 16S rRNA sequencing. The serum levels of inflammatory cytokines (IFN-γ, TNF-α, IL-17, IL-10), AChR-Ab, and LPS were measured using the ELISA method. Colon tissues were subjected to Hematoxylin and eosin (H&E) staining, and Claudin-1 and Muc2 expression was analyzed via immunofluorescence. A microbiota disorder animal model was established by administering an antibiotic mixture via gavage, followed by fecal microbiota transplantation. Splenic CD3+CD4+IL-17A+ Th17 cells and CD3+CD4+CD25+Foxp3+ Treg cells were quantified by flow cytometry. Results: 1. Compositional and structural changes of the gut microbiota in EAMG. Compared with HC, the serum levels of IFN-γ, TNF-α, IL-17, and AChR-Ab in EAMG were significantly increased (P < 0.0001), while the serum level of IL-10 was significantly decreased (P < 0.0001), and the serum level of LPS was increased (P < 0.01). The protein levels of Claudin-1 (P < 0.001) and Muc2 (P < 0.05) in the colon were significantly reduced in EAMG. 2. Relative to rats receiving HC microbiota transplantation (HMb), those receiving EAMG microbiota transplantation (MMb) exhibited significantly elevated serum levels of AChR-Ab (P < 0.01), TNF-α (P < 0.05), IL-17 (P < 0.05), and LPS (P < 0.01), alongside significantly reduced colonic levels of Claudin-1 (P < 0.05) and Muc2 (P < 0.0001). 3. Compared with the EAMG group, the ABX + EAMG group (EAMG with microbiota dysbiosis) exhibited significantly lower colonic levels of Claudin-1 and Muc2 (P < 0.05), a significantly greater splenic Th17/Treg cell imbalance (P < 0.01), and significantly higher serum AChR-Ab levels (P < 0.01). Discussion: The gut microbiota is intricately linked to the progression of EAMG. Microbiota dysbiosis can exacerbate intestinal barrier damage in EAMG and may further influence the pathological changes of myasthenia by disrupting the Th17/Treg immune balance. These findings suggest a novel therapeutic strategy for the treatment of myasthenia gravis by re-establishing microbial homeostasis.
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