<i>Update</i>: The Effect of Interleukin-1 on the Thyroid Gland

Ak, Rasmussen; Feldt‐Rasmussen, Ulla; Bendtzen, Klaus

doi:10.3109/08916939308993319

Cited by 36 publications

(20 citation statements)

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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: 74%

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: 74%

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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“…33 On the other hand, 18.6/NA 199/NA none NA NA= not available; Foll ad = follicular adenoma; *presence or absence of statistically significant difference between studied patient population and control group and with a p value of 0.05; **Hashimoto's thyroiditis + solitary cold nodule Although radioiodine therapy for GD has been suspected of giving rise to cancer development, it seems to be a safe treatment not associated with a significant increase in total cancer mortality. 32 It might, however, be associated with an increased incidence of thyroid cancer, though this is not really substantiated by available studies.…”

Section: Do Thyroid Cancer and Autoimmunity Coexist?mentioning

confidence: 99%

Autoimmunity in differentiated thyroid cancer: Significance and related clinical problems

Feldt‐Rasmussen¹,

Rasmussen²

2010

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coexistence of differentiated thyroid cancer (Dtc) and thyroid autoimmune diseases could represent a mere coincidence due to the frequent occurrence of autoimmunity, but there may also be a pathological and causative link between the two conditions. the coincidence of Dtc with Hashimoto's disease has been variably reported at between 0.5 and 22.5 % and of Dtc with Graves' disease between 0 and 9.8 %. In this review available evidence for thyroid autoimmunity in Dtc is summarized and it is concluded that thyroid cancer does coexist with thyroid autoimmunity, implying that patients treated for autoimmune thyroid diseases should have a careful follow-up. Furthermore, the presence of thyroglobulin antibodies (tgAb) in patients with Dtc may limit the use of serum thyroglobulin as a tumor marker due to methodological problems in the determination of serum thyroglobulin. However, in such cases serial tgAb measurements may be used as a surrogate marker for recurrence of thyroid cancer during the long-term monitoring of Dtc patients.

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“…on thyroid cell viability (Rasmussen et al 1993, MandrupPoulsen et al 1996, Nilsson et al 1998, Bretz et al 1999. The sensitivity of cells to the deleterious effects of cytokines may in fact depend upon the target organ but also on the species, and even on the strain of experimental animals (Eizirik et al 1993.…”

Section: Figurementioning

confidence: 99%

Nitric oxide is involved in interleukin-1alpha-induced cytotoxicity in polarised human thyrocytes

Hove

Stoenoiu²,

Croizet³

et al. 2002

Journal of Endocrinology

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Nitric oxide (NO) is a well-known mediator of autoimmune processes. In the thyroid gland, it is produced in response to interleukin 1 (IL-1) and may mediate cytokine action at an early stage of autoimmune thyroiditis. In this study, we have investigated whether NO is involved in cytokine-induced cytotoxic effects and epithelial barrier alterations in thyrocytes. Human thyroid epithelial cells were cultured as tight polarised monolayers on a permeable support and exposed or not to IL-1 (100 U/ml), alone or in combination with interferon-(IFN-; 100 U/ml) added to the basal compartment. NO production was not detected in control thyrocytes, but was significantly induced by the combination of IL-1 with IFN-, in a time-dependent fashion. Similarly, expression of the inducible isoform of nitric oxide synthase (NOSII), determined by immunoblot and immunofluorescence confocal microscopy, was not detected in control cells, but was markedly induced after 48-h exposure to both cytokines. This treatment significantly increased the release of cytosolic lactate dehydrogenase (LDH) in the apical and basolateral media and decreased transepithelial electrical resistance. Although IFN-was not sufficient to induce NO production, it could by itself decrease transepithelial resistance and synergised the IL-1 effect on LDH release. The NOS inhibitor, -nitro-argininemethyl ester, suppressed the cytokine-induced NO production and decreased the LDH release, but failed to prevent the loss of transepithelial resistance. These results indicated that human thyrocytes express NOSII and produce NO in response to IL-1 +IFN-and suggest that NO acts as a mediator of cytokine-induced cytotoxicity in the thyroid gland and may promote the exposure of autoantigens to the immune system. In contrast, NO does not appear to mediate the cytokine-induced disruption of the thyroid epithelial barrier.

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Update: The Effect of Interleukin-1 on the Thyroid Gland

Cited by 36 publications

References 50 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

Autoimmunity in differentiated thyroid cancer: Significance and related clinical problems

Nitric oxide is involved in interleukin-1alpha-induced cytotoxicity in polarised human thyrocytes

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