Influence of tumour necrosis factor-α, tumour necrosis factor-β and interferon-γ, separately and added together with interleukin-1 β, on the function of cultured human thyroid cells

Rasmussen, Åse Krogh; Kayser, Lars; Feldt‐Rasmussen, Ulla; Bendtzen, Klaus

doi:10.1677/joe.0.1430359

Cited by 57 publications

(38 citation statements)

References 18 publications

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“…Based on these results and data from The observed effects of SHS on thyroid hormone secretion may also reflect the involvement of circulating inflammation markers, and particularly IL-1␤, which have been shown to influence the hypothalamic-pituitary-adrenal axis (23,25). IL-1␤ inhibits differentiated thyroid cell functions (24), including human thyroid cell adenylate cyclase and thyroglobulin release (23,25). Consistent with this notion is the finding that IL-1␤ in our experiment demonstrated significant SHS-induced changes only in men, reflecting an anti-inflammatory effect of estrogens, which is well supported by previous research (28).…”

Section: Discussionmentioning

confidence: 77%

“…Therefore, the observed effects of gonadal hormones may also indicate a downregulating effect on thyroid gland hormonogenesis. Based on these results and data from The observed effects of SHS on thyroid hormone secretion may also reflect the involvement of circulating inflammation markers, and particularly IL-1␤, which have been shown to influence the hypothalamic-pituitary-adrenal axis (23,25). IL-1␤ inhibits differentiated thyroid cell functions (24), including human thyroid cell adenylate cyclase and thyroglobulin release (23,25).…”

Section: Discussionmentioning

confidence: 82%

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Sexual dimorphism in the acute effects of secondhand smoke on thyroid hormone secretion, inflammatory markers and vascular function

Flouris

Metsios²,

Jamurtas³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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Flouris AD, Metsios GS, Jamurtas AZ, Koutedakis Y. Sexual dimorphism in the acute effects of secondhand smoke on thyroid hormone secretion, inflammatory markers and vascular function. Am J Physiol Endocrinol Metab 294: E456-E462, 2008. First published December 11, 2007 doi:10.1152/ajpendo.00699.2007.-Experimental evidence for the physiological effects of secondhand smoke (SHS) is limited, although it affects millions of people globally and its prevalence is increasing, despite currently adopted antismoking measures. Also, scarce evidence suggests that the effects of SHS may be more pronounced in men. We conducted a randomized single-blind crossover study to investigate the sex-specific SHS effects in a controlled simulated bar/restaurant environment on gonadal and thyroid hormones, inflammatory cytokines, and vascular function. Twentyeight (women ϭ 14) nonsmoking adults underwent a 1-h exposure to moderate SHS and a 1-h control trial. Serum and urine cotinine, gonadal and thyroid hormones, inflammatory cytokines, heart rate, and arterial blood pressure were assessed before exposure and immediately after in both trials. Results showed that testosterone (P ϭ 0.019) and progesterone (P Ͻ 0.001) in men and 17␤-estradiol (P ϭ 0.001) and progesterone (P Ͻ 0.001) in women were significantly decreased after SHS. In men, SHS was accompanied by increased free thyroxine (P Ͻ 0.001), triiodothyronine (P ϭ 0.020), and decreased the triiodothyronine-to-free thyroxine ratio (P ϭ 0.033). In women, significant SHS-induced change was observed only in free thyroxine (P ϭ 0.010), with considerable sex variation in free thyroxine and triiodothyronine and a decrease in luteinizing hormone (P ϭ 0.026) and follicle-stimulating hormone (P Ͻ 0.001). After SHS, IL-1␤ (P ϭ 0.001) and systolic blood pressure (P ϭ 0.040) were increased in men but not women. We concluded that a 1-h SHS exposure at bar/ restaurant levels is accompanied by decrements in gonadal hormones in both sexes and marked increases in thyroid hormone secretion, IL-1␤ production, and systolic blood pressure in men.environmental tobacco smoke; cotinine; estrogen; cytokines MORE THAN 126 MILLION AMERICAN and 130 million Chinese adult nonsmokers are currently exposed to secondhand smoke (SHS) on a daily basis, while global estimates include 700 million children and 50 million pregnant women (31). These figures generate major concerns given the overwhelming evidence on the adverse health effects of SHS (26) together with recent reports showing that, despite currently adopted measures, the prevalence rates of smoking are increasing (30). Experimental data from our (17) and other (14,18,19,26) laboratories suggest that even brief exposures to SHS cause marked changes in thyroid hormone secretion, platelet aggregation, endothelial function, arterial pressure waveform, inflammatory markers, as well as other hemodynamic alterations involved in the development of ischemic heart disease. At least some of these effects appear to be more pronounced in men compared with women (14, 20),...

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Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 82%

Sexual dimorphism in the acute effects of secondhand smoke on thyroid hormone secretion, inflammatory markers and vascular function

Flouris

Metsios²,

Jamurtas³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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“…TNFa plays an important role in the acute phase response and is known to inhibit the TSH-induced cAMP response and Tg production (Deuss et al 1992) and release (Poth et al 1991, Rasmussen et al 1994 in cultured thyrocytes. TNFa also inhibits NIS expression in rat FTRL-5 cells (Ajjan et al 1998).…”

Section: The Effect Of Cytokines On Th Synthesismentioning

confidence: 99%

The molecular basis of the non-thyroidal illness syndrome

Vries¹,

Fliers²,

Boelen³

2015

Journal of Endocrinology

152

116

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The 'sick euthyroid syndrome' or 'non-thyroidal illness syndrome' (NTIS) occurs in a large proportion of hospitalized patients and comprises a variety of alterations in the hypothalamus-pituitary-thyroid (HPT) axis that are observed during illness. One of the hallmarks of NTIS is decreased thyroid hormone (TH) serum concentrations, often viewed as an adaptive mechanism to save energy. Downregulation of hypophysiotropic TRH neurons in the paraventricular nucleus of the hypothalamus and of TSH production in the pituitary gland points to disturbed negative feedback regulation during illness. In addition to these alterations in the central component of the HPT axis, changes in TH metabolism occur in a variety of TH target tissues during NTIS, dependent on the timing, nature and severity of the illness. Cytokines, released during illness, are known to affect a variety of genes involved in TH metabolism and are therefore considered a major determinant of NTIS. The availability of in vivo and in vitro models for NTIS has elucidated part of the mechanisms involved in the sometimes paradoxical changes in the HPT axis and TH responsive tissues. However, the pathogenesis of NTIS is still incompletely understood. This review focusses on the molecular mechanisms involved in the tissue changes in TH metabolism and discusses the gaps that still require further research.

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“…The exact role of this cytokine in the pathogenesis of autoimmune thyroid diseases is still unclear. TNF-receptors have been shown on thyroid epithelial cells and FRTL-5 cells, and a multitude of TNF-in vitro actions have been demonstrated on these cells [1][2][3][4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Expression of tumour necrosis factor-alpha (TNF-α) mRNA and protein in pathological thyroid tissue and carcinoma cell lines

Aust¹,

Heuer²,

Laue³

et al. 1996

Clinical and Experimental Immunology

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There has been much controversy about the presence of TNF‐α within thyroid tissue. We therefore conducted a study to determine if TNF‐α mRNA is present in thyroid tissue and thyroid‐derived cells. Semiquantitative reverse transcriptase‐polymerase chain reaction (RT‐PCR) was employed with a heterologous competitor fragment. Significantly lower levels of TNF‐α mRNA were found in the autonomous nodules from patients with thyroid autonomy (TA; n = 4; 5.7 ± 1.3 arbitrary units (AU) (mean ± s.e.m.); P < 0.03) and in normal thyroid tissue (n = 2, 7.0 ± 3.1 AU) compared with tissue from patients with Graves’ disease (GD; n = 13; 27.9 ± 10.3 AU), non‐toxic multinodular goitre (NTG; n = 5; 20.9 ± 5.8 AU) and perinodular tissue from TA patients (20.3 ± 4.0 AU). Higher levels were detected in tissues from patients with Hashimoto’s thyroiditis (HT; n = 2; 51.3 ± 10.3 AU). Cultures of pure thyroid‐derived fibroblasts (46 ± 18 AU), thyrocytes (33 ± 8 AU), and the anaplastic thyroid carcinoma cell lines 8505 C (39 ± 11 AU), SW 1736 (214 ± 16 AU) and C 643 (3 ± 1 AU) showed significantly lower TNF‐α mRNA levels than thyroid‐derived lymphocytes (1650 ± 32 AU). TNF‐α was detected in the supernatants of unstimulated lymphocytes (22.1 ± 1.1 pg/ml) and SW 1736 cells (3.5 ± 0.9 pg/ml), but not in unstimulated fibroblasts and thyrocytes. Using an intracellular labelling technique in flow cytometry, the immunophenotype of stimulated TNF‐α‐positive lymphocytes was determined as predominantly CD3+CD45RO+. Our results suggest that TNF‐α is present in the thyroid tissue of different thyroid disorders. Thyroid‐derived lymphocytes are potential TNF‐α producers and may thus locally influence thyroid function.

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Influence of tumour necrosis factor-α, tumour necrosis factor-β and interferon-γ, separately and added together with interleukin-1 β, on the function of cultured human thyroid cells

Cited by 57 publications

References 18 publications

Sexual dimorphism in the acute effects of secondhand smoke on thyroid hormone secretion, inflammatory markers and vascular function

Sexual dimorphism in the acute effects of secondhand smoke on thyroid hormone secretion, inflammatory markers and vascular function

The molecular basis of the non-thyroidal illness syndrome

Expression of tumour necrosis factor-alpha (TNF-α) mRNA and protein in pathological thyroid tissue and carcinoma cell lines

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