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Interleukin-6 production by thyroid epithelial cells. Enhancement by interleukin-1
M Diamant1, L Kayser, A K Rasmussen
1Laboratory of Medical Immunology, Rigshospitalet, Copenhagen, Denmark.
Insights
Interleukin-1 (IL-1) significantly boosts interleukin-6 (IL-6) production in human thyroid cells, decreasing cAMP and thyroglobulin. This suggests IL-6 may play a role in autoimmune thyroid diseases.
Area of Science:
- Endocrinology
- Immunology
- Cell Biology
Background:
- Interleukin-1 (IL-1) inhibits thyroglobulin and cAMP in human thyroid cells.
- Tumor necrosis factor-alpha and interferon-gamma enhance IL-1's inhibitory effects.
Purpose of the Study:
- To investigate the effect of IL-1 on interleukin-6 (IL-6) production in human thyroid cells.
- To explore the role of other cytokines in IL-6 production.
- To assess IL-6 production in a rat thyroid cell line.
Main Methods:
- Secondary cultures of human thyroid cells were exposed to recombinant IL-1 alpha and -1 beta.
- Tumor necrosis factor-alpha, -beta, and interferon-gamma were used to assess their effects on IL-6 production.
- The rat thyroid cell line FRTL-5 was cultured and treated with IL-1 beta.
Main Results:
- Recombinant IL-1 alpha and -1 beta significantly increased IL-6 production in a dose-dependent manner.
- This IL-1-induced IL-6 increase was associated with decreased cAMP and thyroglobulin production.
- Tumor necrosis factor-alpha and -beta augmented IL-6 production, but less effectively than IL-1.
- Interferon-gamma did not affect IL-6 production.
- FRTL-5 cells produced IL-6 spontaneously, with enhanced production upon IL-1 beta addition.
Conclusions:
- Interleukin-1 stimulates interleukin-6 production in human thyroid cells, correlating with reduced cAMP and thyroglobulin levels.
- Interleukin-6 may have a pathogenic role in autoimmune thyroid diseases.
Abstract:
Interleukin-1 is a potent inhibitor of thyroglobulin and cAMP production in human thyroid cells and the inhibitory effect is enhanced by tumor necrosis factor-alpha and interferon-gamma. In the present study secondary cultures of human thyroid cells produced interleukin-6 and the production was significantly increased after exposure of the cells to recombinant interleukin-1 alpha and -1 beta. This increase was dose-dependent and concomitant of the IL-1 induced decrease in cAMP and thyroglobulin production. Both tumor necrosis factor-alpha and -beta also augmented interleukin-6 production, but less potently than interleukin-1. Interferon-gamma did not affect the production of interleukin-6. The rat thyroid cell line FRTL-5 produced interleukin-6 spontaneously, and the production was enhanced after addition of recombinant interleukin-1 beta. A pathogenetic role of interleukin-6 in autoimmune thyroid disease is suggested.
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