Evidence map›Paper›PMID 42039746›Full record

ArticleFrontiers in cellular and infection microbiology2026

Disruption of intestinal barrier and immune homeostasis links gut microbiota dysbiosis to aggravated experimental autoimmune myasthenia gravis.

Wenqi Tian, Shanshan Peng, Fanfan Xu, Xiaotong Kong, Ying Li, Wei Zhang, Zhaojun Liu, Huixue Zhang, Jianjian Wang, Lihua Wang

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Microorganisms · 2026
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Wenqi TianDepartment of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Shanshan PengDepartment of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Fanfan XuDepartment of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Xiaotong KongDepartment of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Ying LiDepartment of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Wei ZhangDepartment of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Zhaojun LiuDepartment of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Huixue ZhangDepartment of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Jianjian WangDepartment of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Lihua WangDepartment of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

DysbiosisGastrointestinal MicrobiomeHomeostasisMyasthenia Gravis, Autoimmune, ExperimentalAnimalsColonCytokinesDisease Models, AnimalFecal Microbiota TransplantationFemaleIntestinal Barrier FunctionIntestinal MucosaRatsRats, Inbred LewRNA, Ribosomal, 16STh17 CellsCytokinesRNA, Ribosomal, 16Sexperimental autoimmune myasthenia gravis(EAMG)fecal microbiota transplantation (FMT)gut microbiotaintestinal barrierTh17/Treg cell

Identifiers

PMID42039746
PMCPMC13106172

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.