Department of Endocrinology and Metabolism, The First Affiliated Hospital of China Medical University, China Medical University, Shenyang, China.
Commun Biol. 2024 Jan 29;7(1):136. doi: 10.1038/s42003-024-05813-6.
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.
桥本甲状腺炎(HT)是一种与碘摄入有关的器官特异性自身免疫性疾病。新出现的证据强调了肠道微生物群通过微生物群-肠道-甲状腺轴在 HT 发病机制中的作用。然而,碘摄入如何改变微生物群并引发 HT 的过程尚不清楚。本研究通过招募 23 名桥本甲状腺炎患者和 25 名健康个体,评估肠道微生物群组成和代谢特征,研究碘如何影响肠道失调和桥本甲状腺炎。此外,我们使用 NOD.H-2h4 小鼠建立了一种自发性发展的甲状腺炎小鼠模型,强调了碘摄入对 HT 进展的影响。根据富集结果,这两组之间的丁酸代谢有显著差异,与健康个体相比,桥本甲状腺炎患者的丁酸显著减少。过量碘摄入引起的肠道菌群失调通过减少丁酸来破坏 TH17/Treg 平衡。总之,碘摄入改变了肠道微生物群组成和代谢变化,影响了微生物群-肠道-甲状腺轴。