LIPOPOLYSACCHARIDE INDUCES AN INCREASE OF SODIUM-IODIDE SYMPORTER (NIS) GENE EXPRESSION AT TRANSCRIPTIONAL LEVEL IN FRTL-5 THYROID CELLS

NICOLA, JUAN PABLO; VÉLEZ, MARIA LAURA; KIMURA, ETNA; FOZZATTI, LAURA; LUCERO, ARIEL MAXIMILIANO; MASINI-REPISO, ANA MARIA

Buenos Aires.

Congreso; 13th INTERNATIONAL THYROID CONGRESS; 2005

Sociedad Latinoamericana de Tiroides (SLAT), AOTA, ATA y ETA.

Lipopolysaccharide (LPS) is an endotoxin present in blood during certain infectious processes. LPS activates gene expression in several cell types and is considered an immunostimulatory agent. First step in thyroid hormonogenesis involve iodide uptake by the sodium iodide symporter (NIS). Controversial reports have examined NIS as an autoantigen in autoimmune thyroid disease. Previous results from our group demonstrated an stimulation of iodide uptake by LPS in FRTL-5. In order to explore the mechanism involved in LPS-induced increase of iodide uptake, the effect of LPS on NIS gene expression was analyzed in TSH (0.5mIU/ml) stimulated FRTL-5 cells. Iodide uptake (131I) was increased by LPS (0.01-1ug/ml) with maximun at 0.1ug/ml at 48h (24-72h) in TSH treated cells. An increment of NIS level was detected by immunofluorescence with laser confocal microscopy at 48h of LPS treatment. In cells transfected with NIS promoter region (-2841 to +13 bp) linked to luciferase gene, LPS increased the TSH-induced functional activity in a concentration and time-dependent manner at 18-24h and decreased it at 48h. Preliminary observations indicated that LPS increased NIS mRNA level (12h). LPS produced an increase of NIS level which could explain, at least in part, the endotoxin-induced stimulation of iodide uptake. The stimulatory action of LPS on NIS gene expression seems to be mediated by transcriptional activation. Since NIS is an important key in the thyroid hormone biosynthesis and a possible autoantigen, these findings support the potential ability of LPS to alter thyroid function.