Abstract
Myasthenia gravis (MG) is an autoimmune-mediated disorder, the etiology of which involves both environmental factors and genetics. While the exact factors responsible for predisposition to MG remain elusive, it is hypothesized that gut microbiota play a critical role in the pathogenesis of MG. This study investigated whether gut microbiota are altered in MG patients by comparing the fecal microbiota profiles of MG patients to those of age- and sex-matched healthy controls. Phylotype profiles of gut microbial populations were generated using hypervariable tag sequencing of the V4 region of the 16S ribosomal RNA gene. Fecal short-chain fatty acids (SCFAs) were assessed by gas chromatographic analyses. The results demonstrated that, compared to the healthy cohort, the gut microbiota of the MG group was changed in terms of the relative abundances of bacterial taxa, with sharply reduced microbial richness, particularly in the genus Clostridium. The fecal SCFA content was significantly lower in the MG group. Furthermore, microbial dysbiosis was closely related to the levels of inflammatory biomarkers in the sera of MG patients.
Highlights
Myasthenia gravis (MG) is an antibody-mediated, T cell-dependent autoimmune disease
Our results provide the first evidence that MG disease features a dysbiotic microbiota with an overall depletion of microbial diversity, as well as an altered structure of the microbial community
Levels of commensal microbe-derived short-chain fatty acids (SCFAs) were significantly lower in MG patients
Summary
Myasthenia gravis (MG) is an antibody-mediated, T cell-dependent autoimmune disease. It is characterized by fluctuating weakness of skeletal muscles, mainly caused by autoantibodies directed against the acetylcholine receptor (AChR) located in the postsynaptic membrane at the neuromuscular junction. Several studies have revealed that the production of AChR antibodies is associated with the disequilibrium of Th1, B cells, and Foxp3+ T regulatory (Treg) cells (Mu et al, 2009; Aricha et al, 2011). In patients with MG, the frequency of Foxp3+ CD4+ Treg cells is significantly deficient and has become the major focus of many studies on the pathogenesis of MG (Fattorossi et al, 2005; Li et al, 2008; Masuda et al, 2010). Novel approaches that can restore the defects in Foxp3+ CD4+ Treg cell numbers will be valuable for the treatment of MG disease
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