Association between autoimmune thyroiditis and gut microbiota

Autoimmune thyroiditis (AIT) is characterized by thyroid dysfunction and immune disorders. AIT is a T-cell-media­ted, organ-specific autoimmune disease caused by interactions between genetic and environmental factors. Patients with AIT show thyroid lymphocyte infiltration and increased thyroid autoimmune antibodies, thereby altering the integrity of thyroid follicular epithelial cells and dysregulating their metabolism and immune function, leading to a decrease in multitissue metabolic activity. Growing attention has been paid toward the state of gut microbiota over the last few decades. Several recent studies have found that gut microbiota composition in patients with AIT has altered. Recent studies have revealed that gut microbiota is involved in the occurrence and development of AIT by influencing the gut-thyroid axis. We conducted a search in the PubMed, Web of Science, Embase, and Cochrane databases. The analysis showed that the diversity and abundance of certain gut micro­biota were changed in patients with AIT compared to the control group. Chao1, the index of microflora richness, increased in the AIT group compared to controls. Some beneficial bacteria such as Bifidobacterium and Lactobacillus decreased in AIT patients, and harmful microbiota like Bacteroides fragilis significantly increased compared to the control group. The percentage of other bacteria such as Bacteroidetes, Bacteroides, and Lachnospiraceae increased compared to controls. The bacterial abundance and diversity in patients with AIT reduced significantly, and the relative amount of Bacteroides, fecal Bacillus, Prevotella, and Lactobacillus also decreased. The confirmation of whether adjusting the composition of the gut microbiota can improve outcomes in patients with AIT is still pending. This analysis indicates an association between AIT and alteration of microbiota composition. The influence of microbiota on the absorption of trace elements necessary for normal thyroid function is shown.