Abstract
Hashimoto thyroiditis (HT) is an organ-specific autoimmune disease linked to iodine intake. Emerging evidence highlights the gut microbiota's role in HT pathogenesis via the microbiota-gut-thyroid axis. However, the process through which iodine intake modifies the microbiota and triggers HT remains unclear. This study examines how iodine affects gut dysbiosis and HT, recruiting 23 patients with HT and 25 healthy individuals to assess gut microbiota composition and metabolic features. Furthermore, we establish a spontaneously developed thyroiditis mouse model using NOD.H-2h4 mice highlighting the influence of iodine intake on HT progression. The butanoate metabolism significantly differs between these two groups according to the enrichment results, and butyric acid is significantly decreased in patients with HT compared with those in healthy individuals. Gut dysbiosis, driven by excessive iodine intake, disrupts TH17/Treg balance by reducing butyric acid. In summary, iodine intake alters intestinal microbiota composition and metabolic changes influencing the microbiota-gut-thyroid axis.