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G. D. BROADHEAD
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S. M. DIRMIKIS
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H. HUMPHRIES
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S. K. JUSTICE
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G. LOY
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T. SMITH
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Section of Pharmacology, Academic Division of Medicine and *Field Laboratories, The University, Sheffield, S102TN

(Received 8 July 1975)

The McKenzie (1958) bioassay remains the principal tool for studying the long-acting thyroid stimulator (LATS) and LATS-protector (LATSP), although radioreceptor binding assays are being developed (Manley, Bourke & Hawker, 1974; Smith & Hall, 1974). A dog biscuit met the low-iodine requirements until 1974, when batches contained sufficient iodine to make them unsuitable for use in this bioassay. Bread contains negligible iodine, unless iodated dough conditioner is added (London & Vought, 1965). Thus an investigation was made of the suitability of bread for use in the McKenzie bioassay.

Female, white Swiss mice were bred as described by Loy & Broadhead (1968), the colony being fed on pasteurized breeding diet (Oxoid Ltd). Mice were weaned at 4 weeks, fed on diet 86 (Oxoid Ltd) until body weights were 15–20 g (i.e. usually for 1–2 weeks),

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R. L. Kennedy
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T. H. Jones
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R. Davies
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S. K. Justice
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N. R. Lemoine
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ABSTRACT

Interleukin-6 (IL-6) has actions on a variety of endocrine tissues. The cytokine is secreted by cells of the anterior pituitary and endocrine pancreas and has recently been shown to be produced by cultures of thyroid epithelial cells. In this study we have examined some of the factors which regulate IL-6 release from an immortalized human thyroid line (HTori3).

IL-6 release over 24 h was stimulated by TSH (5000 μU/ml), by forskolin (0·01 mmol/l), by fetal calf serum (1–20%) and by epidermal growth factor (20 ng/ml). Stimulation was also apparent with γ-interferon and with tumour necrosis factor at concentrations known to enhance class II major histocompatibility antigen expression by thyroid epithelium. The most potent factor tested was interleukin-1 (IL-1), which controls IL-6 release from other cell types. Threefold stimulation was found with 1 U/ml rising to 350-fold with 1000 U/ml. The effect of IL-1 took 2 h to develop and was blocked by cycloheximide (100 μmol/l). Stimulation was not markedly inhibited by pertussis toxin. Many of the actions of IL-1 are mediated by prostaglandin E2 (PGE2). At concentrations as low as 30 nmol/l, PGE2 stimulated IL-6 release but the maximum stimulation obtained with PGE2 was only threefold. The effect of IL-1 was not inhibited by indomethacin.

These data provide further evidence that IL-6 is produced by human thyrocytes. The effect of IL-1 has not been demonstrated previously. Stimulation of IL-6 release by IL-1 did not appear to be mediated by prostaglandin. IL-6 may influence hormone release from the thyroid as it does in other tissues. High concentrations of IL-6 in the thyroid may increase infiltration by, and activation of, lymphocytes in patients with autoimmune thyroid disease.

Journal of Endocrinology (1992) 133, 477–482

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