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 Table of Contents  
Year : 2021  |  Volume : 13  |  Issue : 2  |  Page : 244-247  

The prevalence role of monocyte chemoattractant protein-1 in hashimoto's thyroiditis via various stimuli mechanisms

1 Department of Clinical Laboratory Science, College of Pharmacy, University of Al-Mustansiriyah, Baghdad, Iraq
2 Department of Pharmacology and Toxicology, College of Pharmacy, University of Al-Mustansiriyah, Baghdad, Iraq

Date of Submission19-Nov-2020
Date of Decision05-Jan-2021
Date of Acceptance13-Feb-2021
Date of Web Publication26-May-2021

Correspondence Address:
Dr. Israa Burhan Raoof
Department of Clinical Laboratory Science, College of Pharmacy, University of Al-Mustansiriyah, Baghdad
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpbs.JPBS_746_20

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Hashimoto's thyroiditis (HT) is an autoimmune disease occurred at any age especially in the 30 and 50 years of patient, with time thyroid gland is lost its function, as the lymphocytes produce inflammatory cytokines, have a direct effect on the thyroid gland function. The monocyte chemoattractant protein (MCP) produced by the podocyte and monocyte in response to these stimuli and has a role in the feedback based on thyroid hormones therefore MCP is increased secretion depending on thyroid hormones; also it's increased with enlargement of adipocyte tissue, i.e., in patients with high body mass index (BMI), there is a relationship between Hashimoto's disease and obesity, that has an effect on the thyroid gland function. Obesity have important role on thyrostimulated hormones (TSHs), as it has a great effect on metabolism and expansion of the thyroid gland; researchers have previously found that obese individuals have higher serum TSH levels. The results of the study have reported that MCP 1, TSH, and BMI levels were highly significant increased in sera of G2 compared with G1, while T3 and T4 levels were highly significant decreased in sera of G2 compared with G1 in referring to G1: Healthy control group while G2: HT patients.

Keywords: Hashimoto's thyroiditis, monocyte chemoattractant protein, thyrostimulated hormone

How to cite this article:
Raoof IB, Mohsin RA, Okhti ZA. The prevalence role of monocyte chemoattractant protein-1 in hashimoto's thyroiditis via various stimuli mechanisms. J Pharm Bioall Sci 2021;13:244-7

How to cite this URL:
Raoof IB, Mohsin RA, Okhti ZA. The prevalence role of monocyte chemoattractant protein-1 in hashimoto's thyroiditis via various stimuli mechanisms. J Pharm Bioall Sci [serial online] 2021 [cited 2022 Dec 7];13:244-7. Available from:

   Introduction Top

Hashimoto's thyroiditis (HT) was first presented in 1912 by Hakaru Hashimoto. It is a synonym for chronic lymphocytic thyroiditis and autoimmune thyroiditis. Its incidence is about 30–60 each of 100,000 inhabitants per year with a prevalence rate of 1%–4%. It is also the foremost common type of thyroiditis and the second of most common thyroid lesions next to goiter. HT is an autoimmune condition that mainly affects women in the third and fourth decades. Moreover, there is a strong association with antithyroid antibodies, particularly anti-TPO antibodies. Anti-TPO and thyrostimulated hormone (TSH) are essential together, even if there is no lymphocytic infiltration. This can be due to a very early stage of lymphocytic thyroiditis; however, a multidisciplinary approach, involving psychiatric, radiological, biochemical, and cytological criteria, should be used to diagnose subclinical hypothyroid status and includes a therapy guide.[1] Moreover, HT, known as chronic lymphocytic thyroiditis, is caused by an autoimmune response which immune cells increased autoantibodies targeting to thyroid antigens such as thyroid peroxidase and thyroglobulin may development to atrophy and transformation of thyroid cell.[2] The autoimmune reaction is triggered by infiltrating self-reactive T lymphocytes and other components of the immune defense system that constitute an inflammatory infiltrate which, under chronic conditions, leads to thyroiditis and hypothyroidism. In addition to the risk factors for incidence Hashimoto's thyroiditis include environmental factors, such as iodine deficiency and infection, and nonenvironmental risk factors, such as genetic susceptibility, which may be associated with a history of hereditary autoimmune disorders in some cases.[3] Therefore, autoimmune thyroiditis is, thus, a polygenic disorder arising from a complex set of genetic and environmental causes and the function of both is still poorly understood.[4] A number of genetic susceptibility loci associated with autoimmunity have been identified by genome-wide association study, especially with the production of thyroid autoantibodies.[5],[6] Thyroiditis, on the other hand, consists of different disorders marked by thyroid inflammation, and HT is the most prevalent and clinically important form of thyroiditis generally seen in middle-aged women. It has been reported that iodine supplementation in iodine-deficient areas elevates lymphocytic infiltration of the thyroid gland by threefold along with a rise in the plasma levels of antithyroid antibody.[7] Lymphocyte cells may produce inflammatory cytokines in the thyroid tissue by activate macrophage and migration to cause direct effect into the thyroid gland.[8] The monocyte chemoattractant protein-1 (MCP-1) is a potent chemokine. It is synthesized and delivered after hemodynamic stimuli such as blood flow or endothelin-1 by the cardiac, vascular, and renal cells. MCP-1 secretion is influenced by age, body mass index, obesity, and inflammatory diseases, which are note in an experimental studies.[9] There are many articles about the role of MCP-1 in the pathogenesis of several inflammatory diseases elsewhere. In addition to that, macrophage plays a significant function in defense by processing and presenting antigen to lymphocyte or by engaging in efferent limb immune response as an effecter or a secreting cytokine. Inflammatory site of the macrophages is derived from blood monocyte, which are attract by chemotactic factor produce in the inflammatory sites.[10] Inflammatory markers increase the secretion depending on the thyroid hormone under negative feedback control.[11] Protein-structured cytokine plays a key role in the immune responses.[12] Thyroid disorders in patients often have a high risk of other nonthyroid disorders, such as obesity, thereby guiding the effect on thyroid diseases.[13] On the other hand, adipocyte cells involved in the recruitment and activation of peripheral blood leukocyte cells in the adipose tissue which expression and secretion by MCP-1.[14]

   Subjects and Methods Top

Thirty Iraqi patients aged 30–35 years were enrolled in the study and the other thirty were healthy subjects aged 26–32 years enrolled as control groups; hence, the protocol of this study included two groups:

G1: Healthy control group and G2: HT patients.

Practically, T4, T3, TSH, and MCP were identified in the sera of each group.

In both T3, T4, TSH, and MCP, the determination of the enzyme activity in the antibody-bound fraction was measured by the reaction with the substrate, and the color and strength of the substrate were calculated by the sandwich ELISA process.

Statistical analysis

The statistical analysis was expressed using SPSS-18 software including mean ± St and P value (P ≤ 0.05)*, (P ≤ 0.01)** considered as a significant difference as a comparison between patients and healthy subjects (control groups).

   Results and Discussion Top

The clinical description of patients and control subjects is shown in [Table 1].
Table 1: Clinical description of patients and control subjects

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MCP-1 with thyroid hormone in the sera of patients and control subjects is shown in [Table 2].
Table 2: Monocyte chemoattractant protein-1 with thyroid hormone in sera of patients and control subjects

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Chronic autoimmune thyroiditis is the most common cause of hypothyroidism and thyroiditis. It is also referred to as chronic lymphocytic thyroiditis or HT. Up to 95% of cases occur in women.[15] In [Table 2], there was hypothyroidism in patients showed slightly elevated in TSH due to increased antithyroid antibodies. Signs and symptoms of hypothyroidism are the major clinical manifestation.[16],[17] Increase Inflammations in thyroid gland caused damage of thyroid follicle of thyroglobulin storage and TSH secretion from the anterior pituitary in response to disorder in negative feedback inhibition. Typically, T4 is the preferred thyroid hormone test for hypothyroidism.[3] In the [Table 2] showed increased levels of MCP 1 in patients compared with control groups, its one of the main chemokines molecules with powerful chemotactic action for monocyte and macrophage cells at inflammatory site. MCP-1 is produced by several cell types, including mesangial, podocytes, and monocytes, in response to various proinflammatory stimuli such as tumor necrosis factor alpha.[18] The existence of chronic low-grade inflammations with MCP-1 and macrophage inflammatory protein-1 closely linked to metabolic syndrome is emerging.[19] On the other hand, MCP-1 is expressed and secreted by adipocyte cells, which have been reported to be involved in the recruitment and activation of peripheral blood leukocyte cells in adipose tissues.[14] Moreover, the association between obesity and inflammations is very strong, it has been found that the monocyte chemotactic protein 1 (MCP 1) genes is significantly up regulated in obesity obese mice model induction by foods.[20],[21] The two common conditions are obesity and thyroid disorder an intriguing correlation between these two entities so, the results noticed in [Table 1] and [Table 2] are inconsistent for example, researchers have previously found that obese individual have higher serum TSH level,[22] and the mechanism that causes hypothyroidism includes increased weight are expected to be accomplished by energy expenditure and appetite disorders. Obesity is a chronic mechanism of low-grade inflammations; cytokine cells and other inflammatory marker are thus produced by adipose tissue overloading.[23] Increased levels of inflammatory cytokine can inhibit sodium and iodide symporter mRNA expression, and then influence human thyroid cell iodide uptake behaviors. These cytokine cells can also cause vasodilatation and elevated thyroid gland blood vessel permeabilities, resulting in morphological and functional thyroid change. Leptin hormone release by adipocyte cells also played a role in chronic inflammations, which can contribute to morphological change in the thyroid, caused thyroid hormone level change in obese people. Some other studies have found that this chronic inflammation status in obesity can also affect the thyroid functions by modulating the expression and activity. It can clarify in part the mechanism by which obesity can cause hypothyroidism. Nevertheless, the etiologies for the correlation of obesity and hypothyroidism.[24]

   Conclusion Top

Monocytes and podocyte secretion in response to various inflammations and stimuli MCP 1 according to the negative feedback of HT. Obesity is associated with TSH and thyroid gland hormones disorders, which has a direct effect on the thyroid gland function, so inflammation state and obesity playing role to contribute morphological changes of thyroid gland.


I would like to thank Mustansiriyah University for providing incorporeal support to complete the work.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

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Rydzewska M, Jaromin M, Pasierowska I, Stozek K, Bossowski A. Role of the T and B lymphocytes in pathogenesis of autoimmune thyroid diseases. Thyroid Res 2018;11:1-11.  Back to cited text no. 2
Subhi O, Schulten HJ, Bagatian N, Al-Dayini R, Karim S, Bakhashab S, et al. Genetic relationship between Hashimoto's thyroiditis and papillary thyroid carcinoma with coexisting Hashimoto's thyroiditis. PLoS One 2020;15:e0234566.  Back to cited text no. 3
Ishtiaq A. Hashimotos thyroiditis and vit d deficiency. Isra Med J 2014;6:41.  Back to cited text no. 4
Hwangbo Y, Park YJ. Genome-Wide association studies of autoimmune thyroid diseases, thyroid function, and thyroid cancer. Endocrinol Metab (Seoul, Korea) 2018;33:175-84.  Back to cited text no. 5
Brčić L, Barić A, Gračan S, Torlak V, Brekalo M, Škrabić V, et al. Genome-wide association analysis suggests novel loci underlying thyroid antibodies in Hashimoto's thyroiditis. Sci Rep 2019;9:5360.  Back to cited text no. 6
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Singh S, Yazdani U, Gadad B, Zaman S, Hynan LS, Roatch N, et al. Serum thyroid-stimulating hormone and interleukin-8 levels in boys with autism spectrum disorder. J Neuroinflammation 2017;14:113.  Back to cited text no. 11
Priyanka R, Muralidharan NP. Interferons and interferon therapy. J Pharm Sci Res 2014;6:400-3.  Back to cited text no. 12
Baumgartner C, da Costa BR, Collet TH, Feller M, Floriani C, Bauer DC, et al. Thyroid function within the normal range, subclinical hypothyroidism, and the risk of atrial fibrillation. Circulation 2017;136:2100-16.  Back to cited text no. 13
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Gamal A, Eman A, Waleed O, Mohammed M, Heba M. Urinary monocyte chemoattractant Protein -1 as a diagnostic marker of lupus nephritis. Suez Canal Univ Med J 2019;22:122-30.  Back to cited text no. 18
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Journy NM, Bernier MO, Doody MM, Alexander BH, Linet MS, Kitahara CM. Hyperthyroidism, hypothyroidism, and cause-specific mortality in a large cohort of women. Thyroid 2017;27:1001-10.  Back to cited text no. 21
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  [Table 1], [Table 2]


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