Inhibition of human thyroid peroxidase gene expression by interleukin 1

Ashizawa, Kiyoto; Yamashita, Shunichi; Tobinaga, Tamami; Nagayama, Yuji; Kimura, Hironori; Hirayu, Hideshi; Izumi, Motomori; Nagataki, Shigenobu

doi:10.1530/acta.0.1210465

Cited by 37 publications

(14 citation statements)

References 16 publications

(18 reference statements)

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“…Other cases of long latency periods in the appearance of an effect of IL-1 have been reported (Suda et al 1989). This is consistent with the induction of gene transcription and protein synthesis often associated with IL-1 treatment (Raz, Wyche, Siegel & Needleman, 1988;Ashizawa, Yamashita, Tobinaga et al 1989;Horuk & McCubrey, 1989;Suda et al 1989) and the involvement of this mechanism of action in Leydig cells needs to be investigated.…”

Section: Discussionsupporting

confidence: 66%

“…Since there is strong evidence that IL-1-like activity is being produced by testicular cells, probably Sertoli cells, it may well be that IL-1 plays a role in both the paracrine regulation of testicu¬ lar function and in the gonadal response to immune challenge. Such duality in function for IL-1 has already been inferred for other organs (Ashizawa et al 1989;Kordon & Bihoreau, 1989).…”

Section: Discussionsupporting

confidence: 63%

See 1 more Smart Citation

Interleukin-1α-induced changes in androgen and cyclic adenosine 3′,5′-monophosphate release in adult rat Leydig cells in culture

Moore

Moger²

1991

Journal of Endocrinology

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Interleukin-1 (IL-1) has been proposed as a paracrine regulator of testicular function. The effect of this cytokine on adult rat Leydig cells in primary culture was investigated. Interstitial cells were purified on a two-step Percoll gradient and cultured in the presence or absence of recombinant human IL-1 alpha (IL-1 alpha). The presence of IL-1 alpha in the culture media resulted in a dose-dependent increase in 24-h basal androgen release (half-maximal effective concentration = 40-50 U/ml). The stimulatory effect of IL-1 alpha peaked on days 3 and 4, and was often still significant after 6 days of culture. Removal of IL-1 alpha was followed by a return of basal androgen release to control levels within 3 days. In contrast, cells treated with IL-1 alpha (100 U/ml) for 3 days released significantly less androgen (per 4 h) in response to 1-100 ng LH/ml than control cells. A similar inhibitory effect on the response to dibutyryl cAMP and pregnenolone was observed. Under basal conditions, IL-1 alpha-treated cells released significantly more cAMP than did control cells. In contrast, the increase in cAMP release seen with LH-stimulated cells was significantly inhibited by treatment with IL-1 alpha. These results suggest that IL-1 alpha has a dual effect on adult rat Leydig cells in culture. It stimulates basal but inhibits LH-induced androgen release with parallel changes in cAMP levels. An additional inhibitory effect appears to lie at the level of the 17 alpha-hydroxylase/C17-20 lyase enzyme.

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Section: Discussionsupporting

confidence: 66%

Section: Discussionsupporting

confidence: 63%

Interleukin-1α-induced changes in androgen and cyclic adenosine 3′,5′-monophosphate release in adult rat Leydig cells in culture

Moore

Moger²

1991

Journal of Endocrinology

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“…Release of IL-6 in response to IL-1 has been demonstrated in other cell types such as fibroblasts (Sehgal, Walther & Tamm, 1987) and endothelial cells (Shalaby, Waage & Espevik, 1989) although IL-1 did not stimulate IL-6 release from anterior pituitary cells (Spangelo et al 1990¿>). IL-1 increases proliferation of thyrocytes (Mine, Tramontano, Chin & Ingbar, 1987;Kawabe, Eguchi, Shimomura et al 1989), but inhibits cAMP accumu¬ lation (Rasmussen, Bech, Feldt-Rasmussen et al 1988), iodide organification (Sato, Sato, Shizume et al 1990), thyroid peroxidase gene expression (Ashizawa, Yamashita, Tobinaga et al 1989), thyroglobulin production (Rasmussen et al 1988) and phagocytosis (Matsunaga, Eguchi, Fukuda et al 1988). IL-6 shows synergy with IL-1 in many of the actions of the latter in immune cells and, in some cases, IL-6 may be a mediator of the actions of IL-1 (van Snick, 1990).…”

Section: Resultsmentioning

confidence: 99%

“…IL-6 shows synergy with IL-1 in many of the actions of the latter in immune cells and, in some cases, IL-6 may be a mediator of the actions of IL-1 (van Snick, 1990). The documented actions of IL-6 on thyroid epithelial cells are shared by IL-1 (Rasmussen et al 1988;Ashizawa et al 1989), and IL-6 may mediate some of the effects of IL-1 on the thyroid.…”

Section: Resultsmentioning

confidence: 99%

Release of interleukin-6 by human thyroid epithelial cells immortalized by simian virus 40 DNA transfection

Kennedy

Jones²,

Davies³

et al. 1992

Journal of Endocrinology

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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 microU/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 gamma-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 mumol/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.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…More than 20 years ago (1987), we reported in vitro data showing that IFN-g inhibited thyroid hormone synthesis in monolayer cultures of human thyroid cells (3). Our subsequent studies published in the late 1980s and early 1990s also demonstrated suppression by various cytokines (interleukin [IL]-1, IL-6, and IFN-g) of thyroid-specific gene expression, including the thyrotropin receptor, thyroid peroxidase, and thyroglobulin (4)(5)(6)(7)(8), indicating cytokine-mediated inhibition of thyroid function. In addition, a series of articles by Sato and colleagues (9)(10)(11) reported inhibition of iodine incorporation, iodine organification, and thyroid hormone synthesis by various cytokines (IL-1, IL-2, tumor necrosis factor-a, IFN-a, and IFN-g) in human thyroid cell suspension cultures.…”

mentioning

confidence: 94%

Inhibition of human thyroid peroxidase gene expression by interleukin 1

Cited by 37 publications

References 16 publications

Interleukin-1α-induced changes in androgen and cyclic adenosine 3′,5′-monophosphate release in adult rat Leydig cells in culture

Interleukin-1α-induced changes in androgen and cyclic adenosine 3′,5′-monophosphate release in adult rat Leydig cells in culture

Release of interleukin-6 by human thyroid epithelial cells immortalized by simian virus 40 DNA transfection

Observations on the Proposed “Nonclassical” Model of Autoimmune Hypothyroidism

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