Gut Microbiome and Autoimmune Thyroid Diseases: New Pathogenetic Mechanisms and Therapeutic Perspectives
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Abstract
This article systematically examines the bidirectional pathogenetic relationship between the gut microbiome and autoimmune thyroid diseases, primarily Hashimoto's thyroiditis (HT) and Graves' disease (GD). Fundamental and clinical research conducted over the past decade demonstrates that quantitative and qualitative changes in the gut microbiota — dysbiosis — may constitute a critical triggering factor for thyroid autoimmunity. The article highlights three principal mechanisms: (1) increased intestinal epithelial permeability and the "leaky gut" phenomenon; (2) functional suppression of T-regulatory cells (Treg) under dysbiotic conditions; and (3) immune modulation mediated by short-chain fatty acids (SCFAs) and lipopolysaccharides (LPS). In addition, the findings of comparative metagenomic studies using 16S rRNA sequencing, clinical data on the reduction of TPO-antibody titers through probiotic intervention (Lactobacillus, Bifidobacterium), and the prospects of fecal microbiota transplantation (FMT) are discussed in detail. In conclusion, the "gut-thyroid axis" concept opens a new window in endocrinology practice: monitoring of the gut microbiota may play an important role in the early diagnosis of autoimmune thyroid diseases, in reducing antibody titers, and in future personalized therapy.
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References
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