scholarly journals Interleukin-6 (IL-6) inhibits thyroid function in the presence of soluble IL-6 receptor in cultured human thyroid follicles.

Endocrinology ◽  
1996 ◽  
Vol 137 (11) ◽  
pp. 4857-4863 ◽  
Author(s):  
K Yamazaki ◽  
E Yamada ◽  
Y Kanaji ◽  
K Shizume ◽  
D S Wang ◽  
...  
Author(s):  
Sarai Keestra ◽  
Vedrana Högqvist Tabor ◽  
Alexandra Alvergne

Abstract Two hundred million people worldwide experience some form of thyroid disorder, with women being especially at risk. However, why human thyroid function varies between populations, individuals and across the lifespan has attracted little research to date. This limits our ability to evaluate the conditions under which patterns of variation in thyroid function are best understood as ‘normal’ or ‘pathological’. In this review, we aim to spark interest in research aimed at understanding the causes of variation in thyroid phenotypes. We start by assessing the biomedical literature on thyroid imbalance to discuss the validity of existing reference intervals for diagnosis and treatment across individuals and populations. We then propose an evolutionary ecological framework for understanding the phylogenetic, genetic, ecological, developmental and physiological causes of normal variation in thyroid function. We build on this approach to suggest testable predictions for how environmental challenges interact with individual circumstances to influence the onset of thyroid disorders. We propose that dietary changes, ecological disruptions of co-evolutionary processes during pregnancy and with pathogens, emerging infections and exacerbated stress responses can contribute to explaining the onset of thyroid diseases. For patients to receive the best personalised care, research into the causes of thyroid variation at multiple levels is needed.


1959 ◽  
Vol 19 (1) ◽  
pp. 28-34 ◽  
Author(s):  
JERZY EINHORN ◽  
LARS-GUNNAR LARSSON

2014 ◽  
Vol 30 (4) ◽  
pp. 317-321 ◽  
Author(s):  
Mohamed Elfadil Mohamed Gar-Elnabi ◽  
Reham Mohd Taha ◽  
Mohammed Ahmed Ali Omer ◽  
Mohamed Farahna ◽  
Yahia M. Bushara

1994 ◽  
Vol 1 ◽  
pp. 494
Author(s):  
Y. Hirooka ◽  
T. Mitsuma ◽  
T. Nogimori ◽  
T. Naruse ◽  
A. Koike ◽  
...  

2009 ◽  
Vol 97 (02/03) ◽  
pp. 179-181 ◽  
Author(s):  
A. Krogh Rasmussen ◽  
L. Kayser ◽  
Ulla Feldt-Rasmussen ◽  
K. Bech ◽  
K. Bendtzen ◽  
...  

2021 ◽  
Vol 78 (4) ◽  
pp. 104-109
Author(s):  
Yuliia Kurylko ◽  
Nataliya Malova ◽  
Larisa Sirotenko

The development of new methods for the treatment of autoimmune thyroid disease is an actual problem of endocrinology. The aim of research was studying of the cell-free effect biological product of cord blood with immunomodulatory properties "Cryocell-Cryocord " on rats’ thyroid function with AIT simulated at an early period of the study. Simulation of autoimmune thyroiditis was carried out by immunization with a suboperatively isolated human thyroid antigen in combination completing Freund's adjuvant on 30 adult male rats weighing 130 - 150 g. Correction was carried out by parenteral ingection of the "Cryocell-Cryocord". Hormonal research (determination of the content of thyroid hormones and antibodies to thyroglobulin (TG-AT) were effected by using standard test kits for enzyme-linked immunosorbent assay at early stages after exposure (7 days, 1 month). Statistical maintained of the results was carried out using the methods of variation statistics. It was used normal distribution to unpaired Student's test to compare indicators. The difference was considered significant at p<0.05. It has been shown the biological preparation of cord blood "Cryocell - Cryocord" has a positive effect with induced autoimmune thyroiditis. It has been noted the normalizing result of the effected correction on the thyroid function of animals in the early period of the studying. It has been proved after the introduction of the biological preparation "Cryocell - Cryocord" in animals with experimental autoimmune thyroiditis observed the inhibition of the manifestations of autoimmune aggression and the normalization of the functional activity of the thyroid gland. These investigations can be the foundation for the development of a new approach to the treatment of patients.


1995 ◽  
Vol 15 (1) ◽  
pp. 11-21 ◽  
Author(s):  
P F Watson ◽  
A P Pickerill ◽  
R Davies ◽  
A P Weetman

ABSTRACT It has been suggested that the thyroid itself may contribute to the inflammatory process observed in autoimmune thyroiditis by releasing the cytokines interleukin-1α (IL-1α), interleukin-6 (IL-6) and interleukin-8 (IL-8), but studies of cytokine gene expression in thyrocytes have been limited and conflicting. A semi-quantitative reverse transcription-PCR technique has been used to investigate the expression of IL-1α, IL-6 and IL-8 mRNA in the human thyroid cell line HTori3 and in cultures of primary human thyroid follicular cells (TFCs). Cytokine mRNA levels were examined over a 24-h period, and the modulatory effects of exogenous IL-1α, interferon-γ (IFN-γ) and TSH investigated. Basal expression of IL-1α, IL-6 and IL-8 mRNA was detected in HTori3 and primary TFC cultures. Stimulation with IL-1 (10 U/ml) for 12 h produced an increase in the level of IL-1α mRNA in both primary TFC and HTori3 cultures. IL-6 and IL-8 mRNA levels were increased by the addition of IL-1 in both cell types, and this effect was detected throughout the 24-h time-course. IFN-γ (100 U/ml) had no significant effect on cytokine gene expression. A higher concentration of IFN-γ (500 U/ml) had no significant effect on the expression of IL-1α or IL-8 but produced an increase in the level of IL-6 mRNA in primary cultures and in HTori3 cells. Addition of TSH (1 mU/ml) produced an increase in the level of IL-1α mRNA in primary TFC and HTori3 cells, at 12 and 24 h. TSH had no significant effect on the expression of IL-6 or IL-8 mRNA. These results demonstrate that human TFCs constitutively express IL-1α, IL-6 and IL-8 mRNA and that this expression can be modulated by IL-1, IFN-γ and TSH.


2017 ◽  
Vol 235 (2) ◽  
pp. 153-165 ◽  
Author(s):  
Celia Siu ◽  
Sam Wiseman ◽  
Sitanshu Gakkhar ◽  
Alireza Heravi-Moussavi ◽  
Misha Bilenky ◽  
...  

The thyroid gland, necessary for normal human growth and development, functions as an essential regulator of metabolism by the production and secretion of appropriate levels of thyroid hormone. However, assessment of abnormal thyroid function may be challenging suggesting a more fundamental understanding of normal function is needed. One way to characterize normal gland function is to study the epigenome and resulting transcriptome within its constituent cells. This study generates the first published reference epigenomes for human thyroid from four individuals using ChIP-seq and RNA-seq. We profiled six histone modifications (H3K4me1, H3K4me3, H3K27ac, H3K36me3, H3K9me3, H3K27me3), identified chromatin states using a hidden Markov model, produced a novel quantitative metric for model selection and established epigenomic maps of 19 chromatin states. We found that epigenetic features characterizing promoters and transcription elongation tend to be more consistent than regions characterizing enhancers or Polycomb-repressed regions and that epigenetically active genes consistent across all epigenomes tend to have higher expression than those not marked as epigenetically active in all epigenomes. We also identified a set of 18 genes epigenetically active and consistently expressed in the thyroid that are likely highly relevant to thyroid function. Altogether, these epigenomes represent a powerful resource to develop a deeper understanding of the underlying molecular biology of thyroid function and provide contextual information of thyroid and human epigenomic data for comparison and integration into future studies.


2006 ◽  
Vol 154 (5) ◽  
pp. 599-611 ◽  
Author(s):  
Malene Boas ◽  
Ulla Feldt-Rasmussen ◽  
Niels E Skakkebæk ◽  
Katharina M Main

There is growing evidence that environmental chemicals can disrupt endocrine systems. Most evidence originates from studies on reproductive organs. However, there is also suspicion that thyroid homeostasis may be disrupted. Several groups of chemicals have potential for thyroid disruption. There is substantial evidence that polychlorinated biphenyls, dioxins and furans cause hypothyroidism in exposed animals and that environmentally occurring doses affect human thyroid homeostasis. Similarly, flame retardants reduce peripheral thyroid hormone (TH) levels in rodents, but human studies are scarce. Studies also indicate thyroid-disruptive properties of phthalates, but the effect of certain phthalates seems to be stimulative on TH production, contrary to most other groups of chemicals. Thyroid disruption may be caused by a variety of mechanisms, as different chemicals interfere with the hypothalamic–pituitary–thyroid axis at different levels. Mechanisms of action may involve the sodium–iodide symporter, thyroid peroxidase enzyme, receptors for THs or TSH, transport proteins or cellular uptake mechanisms. The peripheral metabolism of the THs can be affected through effects on iodothyronine deiodinases or hepatic enzymes. Even small changes in thyroid homeostasis may adversely affect human health, and especially fetal neurological development may be vulnerable. It is therefore urgent to clarify whether the animal data showing effects of chemicals on thyroid function can be extended to humans.


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