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[Pubmed] Intestinal flora and metabolite changes: Uncovering pathogenic mechanisms in myasthenia gravis

Posté : 12 juin 2026 12:00
par RSS-Bot

J Neuroimmunol. 2026 Jun 8;419:578996. doi: 10.1016/j.jneuroim.2026.578996. Online ahead of print.

ABSTRACT

OBJECTIVES: The gut microbiota is associated with the occurrence of Myasthenia gravis (MG), but the biological relevance of these associations is often unclear. We conducted a study to determine whether gut microbiota and metabolites are disturbed in individuals with MG.

METHODS: Stool samples were obtained from 50 individuals with MG, and 15 matched healthy controls (HCs). Then, 16S ribosomal RNA gene amplification sequencing and gas chromatography-mass spectrometry were used to investigate the composition and structure of the gut microbiota community and the levels of metabolites in patients with MG and HCs. Clinical characteristics were collected, including clinical scores such as QMG score, MG-ADL score, MG-QOL-15 score, MMT score, and acetylcholine receptor antibody (AChR-Ab) titer levels. These parameters were used to analyze the correlation between distinct flora and clinical features.

RESULTS: We observed pronounced differences in gut microbiota composition between MG patients and HCs. Notably, the association between Streptomyces and MG disease status was consistent and independent of therapeutic interventions. In treatment-naive MG patients, Acinetobacter and Escherichia-Shigella were significantly associated with disease status. Lachnospiraceae was negatively correlated with QMG score, MG-ADL score, MG-QOL-15 score, and AChR-Ab titer, while exhibiting a positive correlation with MMT score. With respect to the metabolome, a panel of specific metabolites effectively distinguished MG patients from HCs.

CONCLUSION: The gut microbiota and their metabolites exert important effects on MG. The microbiota is closely related to clinical indicators, such as the severity of the disease. Intervention with gut microbes in MG patients may be a new treatment strategy.

PMID:42284706 | DOI:10.1016/j.jneuroim.2026.578996


Source: https://pubmed.ncbi.nlm.nih.gov/4228470 ... 7&v=2.20.0