Effects of iodine intake on gut microbiota community and metabolites: interactions between gut dysbiosis and Hashimoto thyroiditis

Abstract

Abstract Hashimoto thyroiditis (HT) is an organ-specific autoimmune disease associated with iodine intake. Increasing evidence suggests that the gut microbiota plays an important role between the gut and thyroid in HT pathogenesis, which is known as the microbiota-gut-thyroid axis. However, the mechanism by which iodine intake alters the microbiota and causes HT remains unclear. Therefore, this study investigated the mechanisms by which iodine intake influences gut dysbiosis and HT. We recruited 23 patients with HT and 25 healthy individuals to investigate alterations in the gut microbiota composition and metabolic characteristics. Furthermore, we established a spontaneously developed thyroiditis mouse model using NOD.H-2h4 mice underlying the influence of iodine intake on HT progression. The butanoate metabolism significantly differed beween these two groups according to the enrichment results, and butyric acid were significantly decreased in patients with HT compared with those healthy individuales. Gut dysbiosis contributes to TH17/Treg imbalance through a pathway regulated by the reduction of butyric acid. We demonstrated that excessive iodine intake significantly altered the composition of the intestinal flora, leading to gut dysbiosis and metabolic changes via the microbiota-gut-thyroid axis.