Hashimoto's thyroiditis (HT) is an organ-specific autoimmune disease in which both genetic predisposition and environmental factors serve as disease triggers. Many studies have indicated that alterations in the gut microbiota are important environmental factors in the development of inflammatory and autoimmune diseases. We systematically performed a comparative analysis of the gut microbiota in HT patients and healthy controls.
We first conducted a cross-sectional study of 28 HT patients and 16 matched healthy controls. Faecal samples were collected, and microbiota were analysed using 16S ribosomal RNA gene sequencing. Second, an independent cohort of 22 HT patients and 11 healthy controls was used to evaluate the diagnostic potential of the selected biomarkers.
Similar levels of bacterial richness and diversity were found in the gut microbiota of HT patients and healthy controls (p = 0.11). A detailed faecal microbiota Mann-Whitney U-test (Q value < 0.05) revealed that the abundance levels of Blautia, Roseburia, Ruminococcus_torques_group, Romboutsia, Dorea, Fusicatenibacter and Eubacterium_hallii_group genera were increased in HT patients, whereas the abundance levels of Faecalibacterium, Bacteroides, Prevotella_9 and Lachnoclostridium genera were decreased. A correlation matrix based on the Spearman correlation distance confirmed correlations among 7 clinical parameters. Additionally, the LEfSe method showed significant differences in 27 genera between the two groups that were strongly correlated with clinical parameters. We used the linear discriminant analysis (LDA) value to select the first 10 species from the 27 different genera as biomarkers, achieving area under the curve (AUC) values of 0.91 and 0.88 for exploration and validation data, respectively.
Characterization of the gut microbiota in HT patients confirmed that HT patients have altered gut microbiota and that gut microbiota are correlated with clinical parameters, suggesting that microbiome composition data could be used for disease diagnosis. Further investigation is required to better understand the role of the gut microbiota in the aetiopathogenesis of HT.