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Article Abstract
The thyroid gland is the body's largest single organ specialized for endocrine hormone production, and still unraveled mechanisms regulate its interaction between the hypothalamic-pituitary-thyroid axis and composition of the gut microbiota: in particular, a disrupted integrity of the intestinal barrier, causing dysbiosis and increasing detrimental substances or reducing beneficial metabolites, such as short-chain fatty acids (SCFAs) with proinflammatory effects, may be crucial for the induction of an autoimmune thyroid disease. More specifically, Lactobacilli and Bifidobacteria have a role in this partnership through a "molecular mimicry" mechanism, as their protein sequences share structural similarity with thyroid peroxidase and thyroglobulin. Lactobacilli can also increase T helper 17 cells, modifying the number of colonic regulatory T cells, largely implicated in the maintenance of immunological tolerance at the gut barrier. Additionally, Blautia and Anaerostipes work beneficially with butyric acid, one of the SCFAs, promoting antimicrobial peptide synthesis from the intestinal cells and bolstering the innate immune system's ability to struggle against pathogens, which can also influence thyroid hormone levels by regulating iodine uptake and metabolism. This review aims to summarize the current knowledge about the contribution of gut microbiota changes in triggering immune abnormalities leading to autoimmune thyroid diseases.
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| http://dx.doi.org/10.1016/j.autrev.2025.103780 | DOI Listing |
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