scholarly journals Expression of Cytokines and Cytokine Receptors-Genes in Patients with Different Forms of Thyroid Pathology in Ukrainian Population

Author(s):  
Iryna Kamyshna ◽  
Aleksandr Kamyshnyi

Abstract Multiple susceptibility genes can be involved in the development of Hashimoto’s thyroiditis. Some of these genes are implicated in other autoimmune diseases, while others are specific to thyroid autoimmune response. 153 patients with thyroid pathology were enrolled in the study (152 women and 1 man, the average age was 46,02±14,3). They were divided into 3 groups: 16 patients with postoperative hypothyroidism; 65 patients with hypothyroidism resulting from autoimmune thyroiditis, and 72 patients with both AIT and elevated serum an anti-thyroglobulin and anti-thyroid peroxidase antibodies. We used a pathway-specific real-time Polymerase chain reaction array to identify and verify cytokines and receptor pathway-associated gene expression in peripheral white blood cells in randomly selected 12 individuals from each group. In the patients with postoperative hypothyroidism and those with hypothyroidism resulting from autoimmune thyroiditis, the expression of Chemokine (C-X3-C motif) receptor 1, Chemokine (C-X-C motif) receptor 4, Interleukin 6, and Interleukin 6 receptor significantly decreased, while the expression of IL6ST and IL10RA increased. In contrast, mRNA levels of Chemokine (C-X3-C motif) receptor 1, Chemokine (C-X-C motif) receptor 4, Interleukin 6, and Interleukin 6 receptor increased in the autoimmune thyroiditis patients with elevated serum anti-thyroglobulin and anti-thyroid peroxidase antibodies, while the expression of Interleukin 6 signal transducer and Interleukin 10 receptor, alpha decreased in this group of patients. The patients with hypothyroidism resulting from autoimmune thyroiditis and patients with elevated serum anti-thyroglobulin and anti-thyroid peroxidase antibodies had significantly lowered expression of Interleukin 10, while the expression of Interleukin 1, beta and Interleukin 1 receptor, type I was elevated. autoimmune thyroiditis and hypothyroidism affect the mRNA-level expression of cytokines and cytokine receptor genes in a gene-specific manner, and these changes to gene expression can be among the triggers of autoimmune inflammation progression in the thyroid gland. Transcriptional activity of cytokines, inducer, and receptor genes in the peripheral white blood cells can be used as an important minimally invasive prognostic marker of the autoimmune thyroid disease severity.

2020 ◽  
Vol 54 (2) ◽  
pp. 109-118 ◽  
Author(s):  
Iryna I. Bilous ◽  
Mykhaylo M. Korda ◽  
Inna Y. Krynytska ◽  
Aleksandr M. Kamyshnyi

AbstractObjective. Thyroid hormones have important actions in the adult brain. They regulate genes expression in myelination, differentiation of neuronal and glial cells, and neuronal viability and function.Methods. We used the pathway-specific real-time PCR array (Neurotrophins and Receptors RT2 Profiler PCR Array, QIAGEN, Germany) to identify and verify nerve impulse transmission pathway-focused genes expression in peripheral white blood cells of patients with postoperative hypothyroidism, hypothyroidism as a result of autoimmune thyroiditis (AIT) and AIT with elevated serum an anti-thyroglobulin (anti-Tg) and anti-thyroid peroxidase (anti-TPO) antibodies.Results. It was shown that patients with postoperative hypothyroidism and hypothyroidism resulting from AIT had significantly lower expression of BDNF and CBLN1. In patients with AIT with elevated serum anti-Tg and anti-TPO antibodies, the expression of GDNF was significantly down-regulated and the expression of PNOC was up-regulated. The expression levels of MEF2C and NTSR1 were decreased in the group of patients with postoperative hypothyroidism and AIT, correspondingly.Conclusions. The results of this study demonstrate that AIT and hypothyroidism can affect the expression of mRNA nerve impulse transmission genes in gene specific manner and that these changes in gene expressions can be playing a role in the development of neurological complications associated with thyroid pathology. Detection of the transcriptional activity of nerve impulse transmission genes in peripheral white blood cells can be used as an important minimally invasive prognostic marker of the risk for developing neurological complications comorbid with thyroid pathology.


2021 ◽  
Vol 10 (18) ◽  
pp. 4142
Author(s):  
Piotr Lorkiewicz ◽  
Napoleon Waszkiewicz

The COVID-19 pandemic is spreading around the world and 187 million people have already been affected. One of its after-effects is post-COVID depression, which, according to the latest data, affects up to 40% of people who have had SARS-CoV-2 infection. A very important issue for the mental health of the general population is to look for the causes of this complication and its biomarkers. This will help in faster diagnosis and effective treatment of the affected patients. In our work, we focused on the search for major depressive disorder (MDD) biomarkers, which are also present in COVID-19 patients and may influence the development of post-COVID depression. For this purpose, we searched PubMed, Scopus and Google Scholar scientific literature databases using keywords such as ‘COVID-19’, ‘SARS-CoV-2’, ‘depression’, ‘post-COVID’, ‘biomarkers’ and others. Among the biomarkers found, the most important that were frequently described are increased levels of interleukin 6 (IL-6), soluble interleukin 6 receptor (sIL-6R), interleukin 1 β (IL-1β), tumor necrosis factor α (TNF-α), interferon gamma (IFN-γ), interleukin 10 (IL-10), interleukin 2 (IL-2), soluble interleukin 2 receptor (sIL-2R), C-reactive protein (CRP), Monocyte Chemoattractant Protein-1 (MCP-1), serum amyloid a (SAA1) and metabolites of the kynurenine pathway, as well as decreased brain derived neurotrophic factor (BDNF) and tryptophan (TRP). The biomarkers identified by us indicate the etiopathogenesis of post-COVID depression analogous to the leading inflammatory hypothesis of MDD.


2006 ◽  
Vol 11 (4) ◽  
pp. 370-374 ◽  
Author(s):  
Felícito García-Alvarez ◽  
Marta Monzón ◽  
José María Grasa ◽  
Antonio Laclériga ◽  
Beatriz Amorena ◽  
...  

Perfusion ◽  
2005 ◽  
Vol 20 (5) ◽  
pp. 263-268 ◽  
Author(s):  
Gianluca Brancaccio ◽  
Emmanuel Villa ◽  
Elia Girolami ◽  
Guido Michielon ◽  
Cristiana Feltri ◽  
...  

Cardiac surgery with cardiopulmonary bypass (CPB) elicits an inflammatory response and has a multitude of biological consequences, ranging from subclinical organ dysfunction to severe multiorgan failure. Pediatric patients are more prone to have a reaction that can jeopardize their outcome. Cytokines are supposed to be important mediators in this response: limiting their circulating levels is, therefore, appealing. We investigated the pattern of cytokine release during pediatric operation for congenital heart anomalies in 20 patients, and the effect of hemofiltration. Tumor necrosis factor a (TNF-α) was elevated after anesthesia induction and showed significant decrease during CPB. Hemofiltration reduced its concentration, but the effect disappeared on the following day. Interleukin-1 (IL-1) increased slowly at the end of CPB and hemofiltration had no effect. Interleukin-6 (IL-6) showed a tendency toward augmentation during rewarming and hemofiltration did not significantly affect the course. Soluble interleukin-6 receptor (sIL-6r) had a pattern similar to TNF-α, but hemofiltration had no effect. On the other hand, interleukin-8 (IL-8) behaved like IL-6. Our findings suggest that baseline clinical status, anesthetic drugs, and maneuvers before incision may elicit a cytokine response, whereas rewarming is a critical phase of CPB. Hemofiltration is effective in removal of TNF-α, but its role is debatable for the control of IL-1, IL-6, sIL-6r and IL-8 levels.


1991 ◽  
Vol 124 (3) ◽  
pp. 290-294 ◽  
Author(s):  
Tan Tominaga ◽  
Shunichi Yamashita ◽  
Yuji Nagayama ◽  
Shigeki Morita ◽  
Naokata Yokoyama ◽  
...  

Abstract. It has been reported that cytokines, especially interleukin 1 and interferon-γ, inhibit the thyroid hormone secretion and the gene expression of human thyroid peroxidase and thyroglobulin. Interleukin 6 has recently been found to be an important cytokine for the regulation of immunoendocrine interaction and intrathyroidal production of interleukin 6 has been reported. Therefore, we investigated the regulation of thyroid hormone secretion and thyroid peroxidase messenger RNA by interleukin 6 in human thyrocytes to clarify further the functional role of interleukin 6 in thyroid glands. Thyrocytes dispersed from Graves' thyroid tissues were incubated with TSH with or without interleukin 6. TSH (5 U/l stimulated the expression of thyroid peroxidase mRNA transcripts (4.0, 3.2, 2.1, and 1.7 kb, respectively), although unstimulated thyrocytes contained the low level of 3.2 kb thyroid peroxidase mRNA transcript. Interleukin 6 (104-105 U/l) inhibited TSH-induced thyroid peroxidase mRNA in a dose-dependent manner, although the basal level of thyroid peroxidase mRNA expression was not suppressed by interleukin 6. Interleukin 6 also inhibited 8-bromo-cyclic adenosine monophosphate-induced thyroid peroxidase mRNA levels. In contrast, the γ-action mRNA hybridization signal was not altered in control or treated cells. Subsequently, interleukin 6 inhibited TSH-induced T3 secretion in a dose-dependent manner after 72 h treatment. However, interleukin 6 did not affect DNA synthesis. Pretreatment with specific antibody against interleukin 6 selectively restored the inhibitory effect of interleukin 6 on thyroid peroxidase gene expression. Our results suggest that interleukin 6 plays an inhibitory role in the thyroid gland, in addition to interleukin 1 and interferon γ.


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