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Oral Microbiota Profile in a Group of Anti-AChR Antibody-Positive Myasthenia Gravis Patients.

ABSTRACT: Myasthenia gravis (MG) is an autoimmune disorder caused by autoantibodies directed against the postsynaptic membrane at the neuromuscular junction. Perturbation of gut microbiota is thought to contribute to the development of MG, as reflected by fecal metabolomic signatures in humans, but there have been few studies on the relationship between oral microbiota profile and MG. The current study evaluated the correlation between oral microbiota composition and diversity and anti-acetylcholinereceptor (AChR) antibody-positive MG by comparing oral microbiota communities of patients (n = 20) and healthy controls (HCs; n = 20) by 16S rRNA gene sequencing. Principal coordinate analysis and Adonis analysis revealed significant differences in oral microflora profile between the twogroups. Compared to HCs, the abundance of the phyla Firmicutes and Actinobacteria and genera Streptococcus, Rothia, and Lachnoanerobaculum was significantly increased whereas that of phyla Proteobacteria and Spirochaetotaand genera Neisseria, Haemophilus, and Treponema was significantly decreased in MG patients. The Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that the biosynthesis of ansamycins and amino acid metabolism pathways were altered in MG. These results indicate that oral microbiota composition is perturbed in patients with anti-AChR antibody-positive MG, providing new potential avenues for targeted therapeutic interventions.

SUBMITTER: Huang C

PROVIDER: S-EPMC9301194 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Neuromuscular transmission failure in myasthenia gravis (MG) is most commonly elicited by autoantibodies (ab) to the acetylcholine receptor or the muscle-specific kinase, constituting AChR-MG and MuSK-MG. It is controversial whether these MG subtypes arise through different T helper (Th) 1, Th2 or Th17 polarized immune reactions and how these reactions are blunted by immunosuppression. To address these questions, plasma levels of cytokines related to various Th subtypes were determined in patients with AChR-MG, MuSK-MG and healthy controls (CON). Peripheral blood mononuclear cells (PBMC) were activated in vitro by anti-CD3, and cytokines were quantified in supernatants. In purified blood CD4+ T cells, RNA of various cytokines, Th subtype specific transcription factors and the co-stimulatory molecule, CD40L, were quantified by qRT-PCR. Plasma levels of Th1, Th2 and Th17 related cytokines were overall not significantly different between MG subtypes and CON. By contrast, in vitro stimulated PBMC from MuSK-MG but not AChR-MG patients showed significantly increased secretion of the Th1, Th17 and T follicular helper cell related cytokines, IFN-γ, IL-17A and IL-21. Stimulated expression of IL-4, IL-6, IL-10 and IL-13 was not significantly different. At the RNA level, expression of CD40L by CD4+ T cells was reduced in both AChR-MG and MuSK-MG patients while expression of Th subset related cytokines and transcription factors were normal. Immunosuppression treatment had two effects: First, it reduced levels of IL12p40 in the plasma of AChR-MG and MuSK-MG patients, leaving other cytokine levels unchanged; second, it reduced spontaneous secretion of IFN-γ and increased secretion of IL-6 and IL-10 by cultured PBMC from AChR-MG, but not MuSK-MG patients. We conclude that Th1 and Th17 immune reactions play a role in MuSK-MG. Immunosuppression attenuates the Th1 response in AChR-MG and MuSK-MG, but otherwise modulates immune responses in AChR-MG and MuSK-MG patients differentially.

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Oral Microbiota Profile in a Group of Anti-AChR Antibody-Positive Myasthenia Gravis Patients.

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