PMID- 2112152
OWN - NLM
STAT- MEDLINE
DCOM- 19900711
LR  - 20181130
IS  - 0021-972X (Print)
IS  - 0021-972X (Linking)
VI  - 70
IP  - 6
DP  - 1990 Jun
TI  - Inhibition of 125I organification and thyroid hormone release by interleukin-1, 
      tumor necrosis factor-alpha, and interferon-gamma in human thyrocytes in 
      suspension culture.
PG  - 1735-43
AB  - To elucidate the mechanism of decreased 131I uptake by the thyroid gland in 
      patients with subacute thyroiditis and painless thyroiditis, human thyroid 
      follicles were cultured with interleukin-1 (IL-1), tumor necrosis factor-alpha 
      (TNF alpha), and/or interferon-gamma (IFN gamma), and the effects of these 
      cytokines on thyroid function were studied in vitro. When human thyrocytes were 
      cultured in RPMI-1640 medium containing 0.5% fetal calf serum and TSH for 5-8 
      days, the cells incorporated 125I, synthesized de novo [125I]iodotyrosines and 
      [125I]iodothyronines, and secreted [125I]T4 and [125I]T3 into the medium. IL-1 
      alpha and IL-1 beta inhibited 125I incorporation and [125I]iodothyronine release 
      in a concentration-dependent manner. The minimal inhibitory effect was detected 
      at 10 pg/ml. Electron microscopic examination revealed a marked decrease in 
      lysosome formation in IL-1-treated thyrocytes. TNF alpha and IFN gamma also 
      inhibited thyroid function in a concentration-dependent manner. Furthermore, when 
      thyrocytes were cultured with IL-1, TNF alpha and IFN gamma, these cytokines more 
      than additively inhibited thyroid function. Although the main mechanism of 131I 
      uptake suppression in the thyroid gland in subacute thyroiditis is due to 
      cellular damage and suppression of TSH release, our present findings suggest that 
      IL-1, TNF alpha, and IFN gamma produced in the inflammatory process within the 
      thyroid gland further inhibit iodine incorporation and at least partly account 
      for the decreased 131I uptake by the thyroid gland in destruction-induced 
      hyperthyroidism.
FAU - Sato, K
AU  - Sato K
AD  - Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's 
      Medical College, Japan.
FAU - Satoh, T
AU  - Satoh T
FAU - Shizume, K
AU  - Shizume K
FAU - Ozawa, M
AU  - Ozawa M
FAU - Han, D C
AU  - Han DC
FAU - Imamura, H
AU  - Imamura H
FAU - Tsushima, T
AU  - Tsushima T
FAU - Demura, H
AU  - Demura H
FAU - Kanaji, Y
AU  - Kanaji Y
FAU - Ito, Y
AU  - Ito Y
AU  - et al.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
RN  - 0 (Interleukin-1)
RN  - 0 (Iodine Radioisotopes)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 06LU7C9H1V (Triiodothyronine)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 9002-71-5 (Thyrotropin)
RN  - Q51BO43MG4 (Thyroxine)
SB  - IM
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Drug
MH  - Humans
MH  - In Vitro Techniques
MH  - Interferon-gamma/*pharmacology
MH  - Interleukin-1/*pharmacology
MH  - Iodine Radioisotopes/*metabolism
MH  - Microscopy, Electron
MH  - Thyroid Gland/cytology/*drug effects/metabolism
MH  - Thyroiditis/metabolism
MH  - Thyrotropin/physiology
MH  - Thyroxine/*metabolism
MH  - Triiodothyronine/*metabolism
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1990/06/01 00:00
MHDA- 1990/06/01 00:01
CRDT- 1990/06/01 00:00
PHST- 1990/06/01 00:00 [pubmed]
PHST- 1990/06/01 00:01 [medline]
PHST- 1990/06/01 00:00 [entrez]
AID - 10.1210/jcem-70-6-1735 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 1990 Jun;70(6):1735-43. doi: 10.1210/jcem-70-6-1735.