The Gut–Thyroid Axis in Hashimoto’s Disease: Evidence of Reduced Short Chain Fatty Acid Producers and Enhanced Virulence Pathways

Hashimoto’s thyroiditis (HT) is one of the most prevalent autoimmune disorders worldwide, yet the environmental triggers driving its progression, especially in the euthyroid state, remain largely elusive. This cross-sectional study investigates the gut–thyroid axis in 20 euthyroid HT patients and 20 matched healthy controls using 16S rRNA gene ribotyping and PICRUSt2 functional profiling. HT patients exhibited significant intestinal dysbiosis, characterized by a marked reduction in microbial diversity and a distinct community structure relative to controls. Taxonomic analysis revealed an expansion of potentially pathogenic taxa, including Staphylococcus aureus, Lawsonella clevelandensis, Prevotella VZCB and Acinetobacter plantarum. Conversely, a significant depletion was observed in key short-chain fatty acid (SCFA)-producing bacteria, specifically within the Faecalibacterium genus (Faecalibacterium PRLD, F. duncaniae, F. prausnitzii, F. hattorii, F. longum). Functional inference using PICRUSt2 suggested an enrichment of predicted pathways involved in bacterial virulence and antimicrobial resistance, including those associated with Staphylococcus aureus infection, staphylococcal enterotoxin production, and β-lactam resistance. Euthyroid HT patients displayed distinct gut microbial alterations and pro-inflammatory functional profiles, suggesting that microbial dysbiosis occurs independently of overt thyroid hormone dysfunction. Targeting the gut microbiome may offer novel avenues for diagnosis, risk stratification, and targeted therapeutic interventions in autoimmune thyroid diseases.