LPS is an endotoxin from Gram-negative bacteria that exerts a wide variety of biological responces and is present in blood during infectious processes. First and main rate-limiting step in thyroid hormonogenesis is the iodide uptake mediated by NIS. Some reports have proposed NIS as an autoantigen in autoimmune thyroid disease. The aim of this work was to analyse the effect of LPS on iodide uptake and NIS gene expression in thyrotropin (TSH) stimulated FRTL-5 cells. Iodide uptake was stimulated by LPS (maximum at 0.1µg/ml, 48h). LPS (0.1µg/ml) increased NIS protein level (immunofluorescence/laser confocal microscopy) after 48h of LPS treatment. In cells transfected with NIS promoter region (-2841 to +13 bp) linked to luciferase gene, LPS increased the promoter activity in a concentration and time-dependent manner at 18-24h. NIS mRNA level was increased by LPS (12h). The expression of LPS receptor TLR4 was evidenced (RT-PCR). In conclusion, LPS is able to stimulate NIS gene expression at transcriptional level. NIS level increment could be involved in the increase of iodide uptake produced by the endotoxin. A novel property of thyroid cell to express TLR4 was revealed. These findings support a potential role of LPS in thyroid pathophysiology.
