Evaluation of the effect of Hashimoto's Thyroiditis on fatty acids involved in inflammation in the thyroid tissue

Abstract

Hashimoto’s thyroiditis (HT) is one of the most common autoimmune diseases associated with inflammation of the thyroid gland. Some fatty acids (FAs) are involved in inflammation. The aim of the study was to investigate how HT affects FA metabolism in thyroid tissue. We examined normal thyroid tissue from 92 patients with and without HT. We determined total FA panel, pro-inflammatory and specialized pro-resolving lipid mediators (SPMs) concentrations and measured the expression levels of genes encoding the corresponding enzymes of FA metabolism and mediator’s synthesis. In HT tissue, we observed increased total lipid levels (p < 0.05), decreased carnitine palmitoyltransferase I (p < 0.05) and increased tumor necrosis factor alpha (p < 0.001) compared to healthy tissue. Simultaneously, we observed an overexpression of enzymes responsible for the synthesis of polyunsaturated FAs and their higher levels in HT tissue. However, despite the overexpression of phospholipase A₂ (p < 0.001), FA translocase CD36 (p < 0.05) and higher levels of free arachidonic acid in HT tissue (p < 0.05), we observed no differences in the expression of COX-2 in both tissues and, interestingly, a downregulation of 15-LOX (p = 0.001) and lower concentrations of SPMs. Finally, the opposite effect of HT on enzymes responsible for anti-inflammatory BCFAs synthesis in mitochondria and cytosol could indicate a compensatory mechanism. To summarize, the mechanism of the effect of HT on FA metabolism is certainly complex. Thyrocytes are perturbed by the inflammatory effects associated with HT, leading to mitochondrial dysfunction and consequently decreased β-oxidation and BCFA metabolism in mitochondria. Furthermore, despite a significant synthesis of PUFAs, SPMs are also not produced.