Dataset Information

Effects of iodine intake on gut microbiota and gut metabolites in Hashimoto thyroiditis-diseased humans and mice.

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.

SUBMITTER: Gong B

PROVIDER: S-EPMC10824742 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature

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Effects of iodine intake on gut microbiota and gut metabolites in Hashimoto thyroiditis-diseased humans and mice.

Gong Boshen B Meng Fanrui F Wang Xichang X Han Yutong Y Yang Wanyu W Wang Chuyuan C Shan Zhongyan Z

Communications biology 20240129 1

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 ...[more]

PMID: 38287080

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Project description:Hashimoto's thyroiditis (HT) is present in the background of around 30% of papillary thyroid carcinomas (PTCs). The genetic predisposition effect of this autoimmune condition is not thoroughly understood. We analyzed the microarray expression profiles of 13 HT, eight PTCs with (w/) coexisting HT, six PTCs without (w/o) coexisting HT, six micro PTCs (mPTCs), and three normal thyroid (TN) samples. Based on a false discovery rate (FDR)-adjusted p-value ≤ 0.05 and a fold change (FC) > 2, four comparison groups were defined, which were HT vs. TN; PTC w/ HT vs. TN; PTC w/o HT vs. TN; and mPTC vs. TN. A Venn diagram displayed 15 different intersecting and non-intersecting differentially expressed gene (DEG) sets, of which a set of 71 DEGs, shared between the two comparison groups HT vs. TN ∩ PTC w/ HT vs. TN, harbored the relatively largest number of genes related to immune and inflammatory functions; oxidative stress and reactive oxygen species (ROS); DNA damage and DNA repair; cell cycle; and apoptosis. The majority of the 71 DEGs were upregulated and the most upregulated DEGs included a number of immunoglobulin kappa variable genes, and other immune-related genes, e.g., CD86 molecule (CD86), interleukin 2 receptor gamma (IL2RG), and interferon, alpha-inducible protein 6 (IFI6). Upregulated genes preferentially associated with other gene ontologies (GO) were, e.g., STAT1, MMP9, TOP2A, and BRCA2. Biofunctional analysis revealed pathways related to immunogenic functions. Further data analysis focused on the set of non-intersecting 358 DEGs derived from the comparison group of HT vs. TN, and on the set of 950 DEGs from the intersection of all four comparison groups. In conclusion, this study indicates that, besides immune/inflammation-related genes, also genes associated with oxidative stress, ROS, DNA damage, DNA repair, cell cycle, and apoptosis are comparably more deregulated in a data set shared between HT and PTC w/ HT. These findings are compatible with the conception of a genetic sequence where chronic inflammatory response is accompanied by deregulation of genes and biofunctions associated with oncogenic transformation. The generated data set may serve as a source for identifying candidate genes and biomarkers that are practical for clinical application.

Dataset Information

Effects of iodine intake on gut microbiota and gut metabolites in Hashimoto thyroiditis-diseased humans and mice.

Publications

Effects of iodine intake on gut microbiota and gut metabolites in Hashimoto thyroiditis-diseased humans and mice.

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