Background: Despite high sensitivity of current assays for autoantibodies to thyroperoxidase (TPO) and to thyroglobulin (Tg), some hypothyroid patients still present with negative tests for circulating anti-thyroid Abs. These patients usually referred to as having seronegative autoimmune thyroiditis (seronegative CAT) have not been characterized, and definite proof that their clinical phenotype is similar to that of patients with classic chronic autoimmune thyroiditis (CAT) is lacking. Objective: To compare the clinical phenotype of seronegative CAT (SN-CAT) and CAT as diagnosed according to a raised serum level of TSH with negative and positive tests for anti-thyroid Abs respectively. Methods: A case-control retrospective study enrolling 55 patients with SN-CAT and 110 patients with CAT was performed. Serum free triiodothyronine (FT 3 ), free thyroxine (FT 4 ), TSH, Tg Abs, and TPO Abs were measured in all patients. Results: Patients with SN-CAT displayed significantly lower mean levels of TSH (6.6G3.4 vs 10.2G9.8 mU/ml; PZ0.009), higher mean FT 4 levels (1.1G0.2 vs 0.9G0.2 ng/dl; PZ0.0002), and similar FT 3 levels when compared with CAT patients. Mean thyroid volume was significantly greater in patients with CAT when compared with SN-CAT patients (11.2G6.5 vs 8.1

Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) are widely used perfluorinated chemicals (PFCs). Previous studies detected PFOA and PFOS in human tissues including the thyroid gland. There are no studies on the in vitro effects of PFOA and PFOS on thyroid cells. Our study was aimed at evaluating the effect of the in vitro exposure to PFOA and PFOS on thyroid cell proliferation and viability. These objectives were investigated using Fisher rat thyroid line-5 (FRTL-5) cells. FRTL-5 cells cultured in the presence of PFOA and PFOS at concentrations up to 10(4) nM do not display changes in their viability and proliferation rate, while at a concentration of 10(5) nM of either PFCs, a significant inhibition of cell proliferation, mainly due to increased cell death, was found. PFOA and PFOS were detected in FRTL-5 cell pellets after 72 h of incubation with PFCs but not in control cultures. When FRTL-5 were incubated with PFCs then washed in PBS and re-cultured for 72 h without PFCs in the medium, no detectable concentrations of PFOA and PFOS were measured in the cell pellet. This indicates that PFOA and PFOS enter thyroid cells by a gradient-based passive diffusion mechanism. Future studies are required to evaluate the potential toxic effect resulting from prolonged in vivo exposure to even lower concentrations of PFCs.

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Interferons (IFNs) and tumor necrosis factor-α (TNF-α) cooperate in activating several inflammation-related genes, which sustain chronic inflammation in autoimmune thyroid disease (AITD). Much is known about the positive signaling of IFNs to activate gene expression in AITD, while the mechanisms by which IFNs negatively regulate genes remain less studied. While IFNs inhibit CXCL8 secretion in several human cell types, their effects on thyroid cells were not evaluated. Our aim was to study the interplay between TNF-α and type I or type II IFNs on CXCL8 secretion by human thyroid cells. CXCL8 was measured in supernatants of primary cultures of thyroid cells basally and after a 24-h incubation with TNF-α. CXCL8 was detected in thyroid cell supernatants in basal conditions (96.2±23.5 pg/mL) being significantly increased (784.7±217.3 pg/mL; P<0.0001 vs. basal) by TNF-α. Twenty-four hour incubation with IFN-γ or IFN-β or IFN-α dose dependently and significantly inhibited both basal and TNF-α-induced CXCL8 secretion. The degree of the inhibitory effect was IFN-γ>IFN-β>IFN-α. This study demonstrates that type I and type II IFNs downregulate both basal and TNF-α-induced CXCL8 secretion by human thyrocytes, IFN-γ being the most powerful inhibitor. Future studies aimed at a better comprehension of the interplay between CXCL8 and thyroid diseases appear worthwhile.