Environmental factors such as bacterial toxins have been proposed to be involved in pathological processes of the thyroid gland. Despite intensive research, little is known about the immunobiology of the thyroid cell and its relation to pathogenesis. Microarray analysis has demonstrated the whole set of Toll-like receptors (TLRs) expression in the thyroid cell, suggesting that these cells could recognize a broad spectrum of microbial molecular patterns.
The main goal of this work was to investigate how thyroid cells respond to LPS as an inflammatory stimulus.
As we previously demonstrated, thyroid cells constitutively express TLR4, MD2 and CD14 at the plasma membrane. TLR4 and MD2 expression, but not CD14 expression, was up-regulated in response to LPS at both mRNA and protein levels measured by RT-PCR and Western Blot. Flow citometry experiments yielded similar results about increased TLR4 and MD2 expression at the plasma membrane. We then investigated whether thyroid cells could respond to LPS regulating the expression of different pro-inflammatory genes. RT-PCR analysis was performed to measure chemokine mRNA levels. LPS treatment increased the mRNA expression of the chemokines CXCL8, CXCL10, CCL2 and CCL5.
Taken together these results indicate that thyroid cells can respond to the inflammatory stimulus of LPS by increasing the expression of its receptor complex and inducing or up-regulating the expression of several chemokine genes. Our results suggest that the thyroid cell is capable of mounting a response to LPS, raising the question whether these cells could turn into active players of the innate immunity, able to initiate an inflammatory process.
