Introduction. Bacterial LPS is an endotoxin that is present in blood during certain infectious processes. LPS activates gene expression in several cell types including the mainly studied immune cells. Because of the immune stimulation, LPS is used in models to induce thyroid autoimmunity. However, LPS action on thyroid function has not been explored. Results from our group previously demonstrated an LPS-induced stimulation of iodide uptake and thyroglobulin expression in FRTL-5 cells.
Objective. Here we study the LPS effect on sodium-iodide symporter (NIS) expression in FRTL-5 thyroid cells.
Results. Iodide uptake (131I) was stimulated by LPS (0.01-1µg/ml, 48 h) with maximum at 0.1µg/ml. The effect varied with time of incubation (24-72 h) with highest value at 48 h. An increase of NIS level was detected by immunofluorescence with laser confocal microscopy after 48 h of LPS (0.01-1µg/ml) treatment. Semiquantitative analysis demonstrated that the maximal effect was observed with 0.1 µg/ml. Values (arbitrary units) were: Basal (B):1.00±0.03, TSH (T):2.52±0.08, TSH+0.01µg/ml LPS (L0.01):4.48±0.09*, TSH+0.1µg/ml LPS (L0.1):5.27±0.24*, TSH+1µg/ml:3.73±0.05* (mean±SEM, *p<0.001 vs T, N=3). In cells transfected with NIS promoter region from –2.841 to +13 linked to luciferase gene, LPS (0.01-0.1µg/ml) increased the TSH-induced transcriptional activity of the construct in a concentration and time-dependent manner (18-24 h) and decreased it at 48 h. Values (arbitrary units) were (18, 24, 48 h): B:1.00±0.09, 1.00±0.02, 1.00±0.38; T:4.27±0.71, 5.26±0.17, 6.31±0.17; L0.01:5.82±0.19*, 9.14±1.35*, 4.91±0.35#; L0.1: 8.09±0.47**, 16.9±1.34**, 3.6±0.19## (mean±SEM, *p<0.05, **p<0.001, #p<0.01, ##p<0.001 vs T, N=3).
Conclusions. The increment in NIS level could explain the increase of iodide uptake induced by the endotoxin. The stimulating effect of NIS expression may be exerted at transcriptional level. Since NIS is an important clue in the biosynthesis of thyroid hormone and also an autoantigen, these findings reveal the potential ability of LPS to alter thyroid function and thyroid-specific gene expression.
