The conspiring role of gut microbiota as primer of autoimmune thyroid diseases: A scoping focus
Linda Sessa, Elena Malavolta, Giorgio Sodero, Clelia Cipolla, Donato Rigante
Abstract
The thyroid gland is the body's largest single organ specialized for endocrine hormone production, and still unraveled mechanisms regulate its interaction between the hypothalamic-pituitary-thyroid axis and composition of the gut microbiota: in particular, a disrupted integrity of the intestinal barrier, causing dysbiosis and increasing detrimental substances or reducing beneficial metabolites, such as short-chain fatty acids (SCFAs) with proinflammatory effects, may be crucial for the induction of an autoimmune thyroid disease. More specifically, Lactobacilli and Bifidobacteria have a role in this partnership through a “molecular mimicry” mechanism, as their protein sequences share structural similarity with thyroid peroxidase and thyroglobulin. Lactobacilli can also increase T helper 17 cells, modifying the number of colonic regulatory T cells, largely implicated in the maintenance of immunological tolerance at the gut barrier. Additionally, Blautia and Anaerostipes work beneficially with butyric acid, one of the SCFAs, promoting antimicrobial peptide synthesis from the intestinal cells and bolstering the innate immune system's ability to struggle against pathogens, which can also influence thyroid hormone levels by regulating iodine uptake and metabolism. This review aims to summarize the current knowledge about the contribution of gut microbiota changes in triggering immune abnormalities leading to autoimmune thyroid diseases. • The human intestine is home to a complex and diverse population of microorganisms, whose members are essential for host's metabolism, thereby creating a mutualistic relationship. • Lactobacilli and Bifidobacteria operate through “molecular mimicry” mechanisms due to a structural similarity of their protein sequences with thyroid peroxidase and thyroglobulin. • Variations in diet and drug abuse may cause gut dysbiosis, and an imbalance in the local microbial community might indirectly interfere with normal thyroid function. • Different studies have shown that gut microbiota alterations may actually orchestrate the development of autoimmunity within the thyroid, and a triggering event might be the breakdown of immune tolerance towards thyroid-specific self-antigens. • The use of probiotics has been found to help reducing levothyroxine dose adjustments and restoring thyroid function in immune-mediated thyroid diseases. • Gut microbiota changes in triggering immune abnormalities related to autoimmune thyroid diseases have not been completely defined, and further data are needed to strengthen our knowledge on this partnership.