Inhibition of sup 125 I organification and thyroid hormone release by interleukin-1, tumor necrosis factor-alpha, and interferon-gamma in human thyrocytes in suspension culture

Journal Article · Fri Jun 01 00:00:00 EDT 1990 · Journal of Clinical Endocrinology and Metabolism; (USA)

DOI:https://doi.org/10.1210/jcem-70-6-1735· OSTI ID:6703792

Sato, K; Satoh, T; Shizume, K; Ozawa, M; Han, D C; Imamura, H; Tsushima, T; Demura, H; Kanaji, Y; Ito, Y ^[1]

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1. Institute of Clinical Endocrinology, Tokyo (Japan)

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.

• OSTI ID: 6703792
• Journal Information: Journal of Clinical Endocrinology and Metabolism; (USA), Vol. 70:6; ISSN 0021-972X
• Country of Publication: United States
• Language: English

Related Subjects

63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
59 BASIC BIOLOGICAL SCIENCES
IODINE 131
UPTAKE
THYROID
RADIONUCLIDE KINETICS
THYROIDITIS
PATHOGENESIS
THYROXINE
SECRETION
TRIIODOTHYRONINE
CELL CULTURES
DOSE-RESPONSE RELATIONSHIPS
ELECTRON MICROSCOPY
GROWTH FACTORS
IN VITRO
INHIBITION
INTERFERON
IODINE 125
LYMPHOKINES
LYSOSOMES
MAN
TRACER TECHNIQUES
AMINO ACIDS
ANIMALS
BETA DECAY RADIOISOTOPES
BETA-MINUS DECAY RADIOISOTOPES
BODY
CARBOXYLIC ACIDS
CELL CONSTITUENTS
DAYS LIVING RADIOISOTOPES
DISEASES
ELECTRON CAPTURE RADIOISOTOPES
ENDOCRINE DISEASES
ENDOCRINE GLANDS
GLANDS
HORMONES
INTERMEDIATE MASS NUCLEI
IODINE ISOTOPES
ISOTOPE APPLICATIONS
ISOTOPES
MAMMALS
MICROSCOPY
MITOGENS
NUCLEI
ODD-EVEN NUCLEI
ORGANIC ACIDS
ORGANIC COMPOUNDS
ORGANIC HALOGEN COMPOUNDS
ORGANIC IODINE COMPOUNDS
ORGANOIDS
ORGANS
PEPTIDE HORMONES
PRIMATES
PROTEINS
RADIOISOTOPES
THYROID HORMONES
VERTEBRATES
560161* - Radionuclide Effects
Kinetics
& Toxicology- Man
550901 - Pathology- Tracer Techniques