Search Results
You are looking at 1 - 2 of 2 items for
- Author: U Feldt-Rasmussen x
- Refine by access: All content x
Search for other papers by Å K Rasmussen in
Google Scholar
PubMed
Search for other papers by L Kayser in
Google Scholar
PubMed
Search for other papers by U Feldt-Rasmussen in
Google Scholar
PubMed
Search for other papers by K Bendtzen in
Google Scholar
PubMed
Abstract
Interleukin (IL)-1, tumour necrosis factor (TNF)-α and interferon (IFN)-γ have been demonstrated in thyroid tissue. We have previously shown that high concentrations of IL-1 inhibit and low concentrations stimulate human thyroid cell function in vitro. In the present study, TNF-α, TNF-β and IFN-γ all inhibited thyroglobulin (Tg) and cAMP production from cultured human thyroid cells. When TNF-α was added simultaneously with IL-1 β, the highest concentration of TNF-α (106 U/l) enhanced the inhibition of Tg and cAMP induced by IL-1β (1–105 U/1). TNF-β had no influence on IL-1β-induced inhibition. IFN-γ (104 U/1) added together with IL-1β in lower concentrations (1—102 U/l) stimulated cAMP production, while at high concentrations of IL-1β (105 U/1), IFN-γ enhanced the inhibitory influence of IL-1 β on Tg production.
The hormones of the immune system, IL-1, TNF and IFN-γ, may thus contribute to the decreased thyroid function characteristic of some thyroid inflammatory diseases.
Journal of Endocrinology (1994) 143, 359–365
Search for other papers by J I Reimers in
Google Scholar
PubMed
Search for other papers by A K Rasmussen in
Google Scholar
PubMed
Search for other papers by A E Karlsen in
Google Scholar
PubMed
Search for other papers by U Bjerre in
Google Scholar
PubMed
Search for other papers by H Liang in
Google Scholar
PubMed
Search for other papers by O Morin in
Google Scholar
PubMed
Search for other papers by H U Andersen in
Google Scholar
PubMed
Search for other papers by T Mandrup-Poulsen in
Google Scholar
PubMed
Search for other papers by A G Burger in
Google Scholar
PubMed
Search for other papers by U Feldt-Rasmussen in
Google Scholar
PubMed
Search for other papers by J Nerup in
Google Scholar
PubMed
Abstract
Interleukin-1β has been implicated as a pathogenic factor in the development of autoimmune thyroiditis. When given for 5 days to normal non-diabetes-prone Wistar Kyoto rats, it decreased plasma concentrations of total tri-iodothyronine and thyroxine and increased plasma TSH. These effects were not prevented by co-injection of nitroarginine methyl ester or aminoguanidine, inhibitors of NO synthases. Exposure to interleukin-1β dose-dependently reduced iodine uptake in FRTL-5 cells, but had no effect on thyroglobulin secretion. Nitrite was not detected in the FRTL-5 cell culture media after exposure to interleukin-1β. However, reverse transcription PCR analysis of mRNA isolated from interleukin-1β-exposed FRTL-5 cells revealed a transitory expression of the inducible NO synthase, which was markedly lower than inducible NO synthase induction in interleukin-1β-exposed isolated rat islets of Langerhans. Co-incubation with the NO synthase inhibitor N G-monomethylarginine did not ameliorate the effect of interleukin-1β on FRTL-5 cell iodine uptake. Furthermore, we demonstrate that daily injections of interleukin-1β for 13 weeks aggravated spontaneous thyroiditis and induced severe hypothyroidism in non-diabetic diabetes-prone BB rats. The data suggest that NO does not mediate interleukin-1β-induced inhibition of rat thyroid function in vivo or in vitro in FRTL-5 cells, and the induction of hypothyroidism by interleukin-1β in diabetes-prone BB rats is speculated to be due to exacerbation of recruitment and activation of intrathyroidal mononuclear cells.
Journal of Endocrinology (1996) 151, 147–157
