Role of the Specialized Pro-resolving Mediator Resolvin D1 in Hashimotoʼs Thyroiditis

Author(s):  
Jing Song ◽  
Rongxin Sun ◽  
Yuanyuan Zhang ◽  
Ying Fu ◽  
Dong Zhao

Abstract Objective Resolvins are produced by the catabolism of polyunsaturated fatty acids (PUFAs) and play vital roles in inflammation resolution. Resolvins have been associated with autoimmune disorders. This study aimed to measure the level of Resolvin D1 (RVD1) in the serum of Hashimoto's thyroiditis (HT) patients and healthy controls (HCs) and to further analyse its correlation with thyroid autoantibodies and inflammatory factors. Methods Sixty-three participants were recruited, namely, 30 untreated HT patients and 33 sex- and age-matched HCs. Serum RVD1 and inflammatory chemokine (MCP-1 and IP-10) levels were measured by ELISA according to the manufacturer’s protocol. Serum total T3 (TT3), TT4, free T3 (FT3), FT4, thyroglobulin antibody (TgAb), thyroid peroxidase antibody (TPOAb) and thyroid-stimulating hormone (TSH) levels were measured using an electrochemiluminescence immunoassay. Thyroid homeostasis parameters, including the thyroid secretory capacity (SPINA-GT), the total deiodinase activity (SPINA-GD), Jostel’s TSH index (TSHI) and the thyrotroph thyroid hormone sensitivity index (TTSI), were calculated. Results Serum RVD1 levels in HT patients (134.76, 85.35–201.36 pg/mL) were significantly lower than those in HCs (187.64, 131.01–326.85 pg/mL) (P=0.004). As the TPOAb level increased, the RVD1 level showed a decreasing trend (P for trend=0.002). Both multinomial and ordinal logistics analyses revealed that serum RVD1 levels were negatively correlated with TPOAb levels in the adjusted models. Moreover, RVD1 showed a negative correlation with the inflammatory chemokine IP-1 0 (r=–0.276, P=0.034), TSHI (r=–0.269, P=0.036) and TTSI (r=–0.277, P=0.031). Conclusions Thyroid autoimmunity may be associated with low levels of RVD1. Decreased RVD1 levels indicate impaired resolution of inflammation in HT patients.

2020 ◽  
Vol 26 (6) ◽  
pp. 595-603
Author(s):  
Yanan Zhang ◽  
Xinmei Huang ◽  
Zaoping Chen ◽  
Qian Yang ◽  
Xiaoying Li ◽  
...  

Objective: Previous studies have reported an association between iron deficiency (ID) and increased thyroid peroxidase antibody (TPO-Ab) during early pregnancy. The objective of this study was to explore the relationship between ID and thyroid dysfunction, as well as thyroid autoantibodies, during the second trimester of pregnancy. Methods: A total of 1,592 pregnant women (13 to 28 weeks gestation) were enrolled in this cross-sectional study. According to serum ferritin (SF) concentrations, they were divided into ID (SF <20 μg/L) or non-ID (SF ≥20 μg/L) groups. Logistic regression analysis was used to evaluate the association between ID and subclinical hypothyroidism (thyroid-stimulating hormone [TSH] >4.0 mIU/L and free thyroxine [FT4] within the reference range) and thyroid autoimmunity. Results: The prevalence of ID was 23.43% (373/1,592). Compared with the non-ID group, the ID group had lower FT4 levels (13.94 pmol/L [8.91 to 29.82 pmol/L] versus 14.63 pmol/L [8.22 to 47.24 pmol/L]; P<.001]) and higher TSH levels (1.85 mIU/L [0.01 to 7.84 mIU/L] versus 1.69 mIU/L [0.01 to 10.2 mIU/L]; P<.05). Logistic regression analysis confirmed ID as a risk factor for increased thyroglobulin antibody (TG-Ab) (odds ratio 1.974; 95% confidence interval 1.065, 3.657; P<.05), but not for subclinical hypothyroidism or increased TPO-Ab. Conclusion: ID is associated with increased TG-Ab during the second trimester of pregnancy. Abbreviations: BMI = body mass index; CV = coefficient of variation; FT4 = free thyroxine; Hb = hemoglobin; ID = iron deficiency; IDA = iron deficiency anemia; SF = serum ferritin; T3 = triiodothyronine; T4 = thyroxine; TAI = thyroid autoimmunity; TG = thyroglobulin; TG-Ab = thyroglobulin antibody; TPO = thyroid peroxidase; TPO-Ab = thyroid peroxidase antibody; TSH = thyroid-stimulating hormone


2011 ◽  
Vol 2011 ◽  
pp. 1-3 ◽  
Author(s):  
Emina Kasumagic-Halilovic ◽  
Asja Prohic ◽  
Begler Begovic ◽  
Nermina Ovcina-Kurtovic

Background. Vitiligo is a common skin disorder characterized by macular depigmentation of the skin. The etiopathogenesis of the disease is still unclear, but there is evidence that autoimmunity and endocrine disfunction may be involved.Objective. The aim of this study was to determine whether vitiligo is statistically associated with thyroid autoimmunity.Method. In a prospective case-control study, we compared the frequency of thyroid autoantibodies (thyroglobulin antibody, anti-Tg and thyroid peroxidase antibody, and anti-TPO) in 33 patients with vitiligo and in 33 healthy volunteers. Thyroid autoantibodies and thyroid hormones (thyroxine (T4), triiodothyronine (T3), and thyroid stimulating hormone (TSH) were measured in all subjects.Results. Thyroid functional abnormalities were found in 6 (18.18%) patients. Anti-Tg and anti-TPO were positive in 9 (27.27%) and 8 (24.24%) patients, respectively. In control group, only one subject (3.03%) had abnormalities in thyroid hormonal status, and two subjects had positive thyroid autoantibodies. Compared with the control group, the frequency of both anti-Tg and anti-TPO was significantly higher in those with vitiligo ().Conclusion. This study shows a significant association between vitiligo and thyroid autoimmunity, and that tests to detect thyroid autoantibodies are relevant in patients with vitiligo.


2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Cheng Han ◽  
Xinghai Xia ◽  
Aihua Liu ◽  
Xiaowen Zhang ◽  
Mi Zhou ◽  
...  

Thyroid hormone (TH) affects many metabolic processes such as promoting oxidation of sugar, fat, and protein in many tissues. Thyroid dysfunction is associated with metabolic disorders. The newly discovered adipocyte- and hepatocyte-derived cytokine, betatrophin, has been reported to be involved in metabolic diseases, but its influence on thyroid dysfunction is uncertain. Therefore, the present study aims to evaluate circulating betatrophin levels in subjects with different thyroid function status and to predict the factors associated with betatrophin levels, especially whether thyroid stimulating hormone (TSH), TH, or thyroid autoantibodies are associated with betatrophin levels. In the study, serum betatrophin was measured in the subjects grouped as overt hypothyroidism (OH), subclinical hypothyroidism (SCH), euthyroid with isolated thyroid peroxidase antibody positivity (isolated Ab), and healthy control (HC), according to their thyroid functions. From our results, we found that betatrophin may be associated with thyroid insufficiency but not thyroid autoimmunity. Thus, when interpreting the results of betatrophin, thyroid functions should also be taken into consideration.


2006 ◽  
Vol 154 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Inge Bülow Pedersen ◽  
Peter Laurberg ◽  
Nils Knudsen ◽  
Torben Jørgensen ◽  
Hans Perrild ◽  
...  

Background: Thyroid autoimmunity is more common in females than in males. One possible explanation for this female preponderance may be the effect of oestrogens on the immune system. It has also been suggested that foetal microchimerism involving transfer of foetal cells into maternal tissue during pregnancy may play an important role. Objective: We investigated the association between the presence of circulating thyroid autoantibodies and previous pregnancy, parity and the use of oral contraceptives (OCs) and hormone replacement therapy (HRT) in a population cohort. Methods: We examined 3712 women randomly selected from the general population. Serum was analysed for thyroid peroxidase antibody (TPO-Ab) and thyroglobulin antibody (Tg-Ab) using assays based on an RIA technique (DYNO test). Data were analysed in logistic regression models to adjust for possible confounders. Women previously treated for thyroid disease or with pregnancy within 1 year prior to the study were excluded from the analyses. Results: In both univariate and multivariate models and whether the presence of TPO-Ab and Tg-Ab was investigated alone or in combination, findings were negative with respect to an association between circulating thyroid antibodies and previous pregnancy, number of pregnancies, parity and previous abortion. There was no association between thyroid autoantibodies and use of OCs. Women aged 60–65 years receiving HRT now or previously had a lower prevalence of Tg-Ab (univariate, P = 0.01; multivariate, P = 0.02). No such association was observed between HRT and TPO-Ab. Conclusion: In this population study there was no association between previous pregnancy, parity and thyroid antibodies, which argues against the role of microchimerism as a trigger of thyroid autoimmunity. Exogenous oestrogens may reduce aspects of autoimmunity.


2014 ◽  
Vol 170 (1) ◽  
pp. 63-67 ◽  
Author(s):  
La-or Chailurkit ◽  
Wichai Aekplakorn ◽  
Boonsong Ongphiphadhanakul

IntroductionAlthough autoimmune thyroid disease is less common in males, it is unclear whether estrogen contributes to the difference in susceptibility among males.ObjectiveTo examine whether circulating estradiol (E2) is related to thyroid autoimmunity in males.Patients and methodsOne-thousand two-hundred and sixty-three males aged 15–94 years were studied. Serum levels of E2, TSH receptor antibody (TRAb), thyroid peroxidase antibody (TPOAb), thyroglobulin antibody (TgAb), free thyroxine (FT4), and TSH were measured by ELISA.ResultsCirculating E2varied widely in males, ranging 18.4–403.7 pmol/l with a mean value of 136.2±51.7 pmol/l. E2increased with age (r=0.18,P<0.001). No relationship between E2and BMI was found. When comparing the difference in E2according to the test results of TRAb, TPOAb, and TgAb, it was found that E2was significantly higher in subjects with positive TRAb (TRAb positive, E2=170.3±59.8 pmol/l; TRAb negative, E2=134.0±50.6 pmol/l;P<0.001). No difference in E2was demonstrated according to the results of TPOAb or TgAb. Logistic regression analysis showed that E2was a determinant of positive TRAb, independent of age and BMI. There was no relationship between serum E2and TSH or FT4. However, E2was negatively related to TSH (r=−0.45,P<0.01) in subjects whose TSH levels fell below the reference range (0.3–4.2 mIU/l).ConclusionHigher circulating E2is related to thyroid autoimmunity in males as reflected by positive TRAb.


2020 ◽  
Author(s):  
Jing Song ◽  
Rongxin Sun ◽  
Yuanyuan Zhang ◽  
Jing Ke ◽  
Dong Zhao

Abstract Objective: Omega-3 polyunsaturated fatty acids (PUFAs) can produce lipid mediators with both anti-inflammatory and pro-resolution properties, including resolvins. Resolvins have been associated with autoimmune disorders. This study aimed to measure the level of resolvin E1 (RVE1) in the serum of Hashimoto's thyroiditis (HT) patients and healthy controls (HCs) and to further analyze its correlation with thyroid autoantibodies and other clinical indicators.Design, patients and measurements: Fifty-seven participants were recruited—30 untreated HT patients and 27 sex‐ and age‐matched HCs. Levels of serum RVE1 were measured by ELISA according to the manufacturer’s protocol. Serum total T3 (TT3), TT4, free T3 (FT3), FT4, thyroglobulin antibody (TgAb), thyroid peroxidase antibody (TPOAb) and thyroid-stimulating hormone (TSH) levels were measured using an electrochemiluminescence immunoassay. Routine biochemical and hemogram tests were performed on each sample.Results: Serum RVE1 levels in HT patients (24.09, 15.76-34.38 pg/mL) were significantly lower than those in HCs (28.51, 20.76-51.23 pg/mL) (P=0.027). As the TgAb level increased, the RVE1 content showed a decreasing trend (P for trend=0.001). Multivariable ordinal logistic regression analysis showed that RVE1 was negatively correlated with increasing TgAb in both the unadjusted (OR=0.9446, 95% CI=0.9111-0.9782, P=0.002) and adjusted models (OR=0.9380, 95% CI=0.8967-0.9811, P=0.005).Conclusions: Decreased RVE1 levels indicate impaired resolution of inflammation in HT patients. RVE1 may be a protective factor for elevated TgAb levels.


2020 ◽  
Vol 20 (10) ◽  
pp. 1711-1718
Author(s):  
Maryam Tohidi ◽  
Aidin Baghbani-Oskouei ◽  
Atieh Amouzegar ◽  
Ladan Mehran ◽  
Fereidoun Azizi ◽  
...  

Background: Dysfunction of the thyroid gland has profound effects on the cardiovascular system. Objective: We aimed to explore the relation of serum thyroid peroxidase antibody (TPO-Ab), as a marker of thyroid autoimmunity with incident hypertension among a euthyroid population. Methods: A total of 3681 participants (1647 men) entered the study. Multivariate Cox proportional hazard models were conducted to estimate the association between TPO-Ab and incident hypertension. Results: The mean age (standard deviation) of the participants was 37.5 (12.8) years. During a median follow-up of 12.2 years, 511 men and 519 women developed hypertension. The multivariable hazard ratios (HRs) and related 95% confidence intervals (CIs) of 1-unit increase in natural logarithm (ln) of TPO-Ab for incident hypertension were 1.09 (1.00-1.19), 1.03 (0.97-1.10), and 1.05 (1.00-1.11) for men, women, and total population, respectively. Moreover, considering the TPO-Ab status as a categorical variable (i.e. TPO-Ab positive or TPO-Ab negative), the multivariate-adjusted HRs (95% CIs) of TPO-Ab positivity for incident hypertension, were 1.33 (0.95-1.85), 1.12 (0.86-1.45) and 1.19 (0.97- 1.46) for men, women, and total population, respectively. Conclusion: Elevated serum TPO-Ab level can contribute to the development of hypertension among euthyroid men during a long follow-up; suggesting a role for thyroid autoimmunity.


Pain Medicine ◽  
2021 ◽  
Author(s):  
Gregory Livshits ◽  
Alexander Kalinkovich

Abstract Objective To present a hypothesis on a novel strategy in the treatment of fibromyalgia (FM). Design A narrative review. Setting FM as a disease remains a challenging concept for numerous reasons, including undefined etiopathogenesis, unclear triggers and unsuccessful treatment modalities. We hypothesize that the inflammatome, the entire set of molecules involved in inflammation, acting as a common pathophysiological instrument of gut dysbiosis, sarcopenia, and neuroinflammation, is one of the major mechanisms underlying FM pathogenesis. In this setup, dysbiosis is proposed as the primary trigger of the inflammatome, sarcopenia as the peripheral nociceptive source, and neuroinflammation as the central mechanism of pain sensitization, transmission and symptomatology of FM. Whereas neuroinflammation is highly-considered as a critical deleterious element in FM pathogenesis, the presumed pathogenic roles of sarcopenia and systemic inflammation remain controversial. Nevertheless, sarcopenia-associated processes and dysbiosis have been recently detected in FM individuals. The prevalence of pro-inflammatory factors in the cerebrospinal fluid and blood has been repeatedly observed in FM individuals, supporting an idea on the role of inflammatome in FM pathogenesis. As such, failed inflammation resolution might be one of the underlying pathogenic mechanisms. In accordance, the application of specialized, inflammation pro-resolving mediators (SPMs) seems most suitable for this goal. Conclusions The capability of various SPMs to prevent and attenuate pain has been repeatedly demonstrated in laboratory animal experiments. Since SPMs suppress inflammation in a manner that does not compromise host defense, they could be attractive and safe candidates for the alleviation of FM symptomatology, probably in combination with anti-dysbiotic medicine.


2021 ◽  
Vol 22 (9) ◽  
pp. 4370
Author(s):  
Cássia de Fáveri ◽  
Paula M. Poeta Fermino ◽  
Anna P. Piovezan ◽  
Lia K. Volpato

The pathogenesis of endometriosis is still controversial, although it is known that the inflammatory immune response plays a critical role in this process. The resolution of inflammation is an active process where the activation of endogenous factors allows the host tissue to maintain homeostasis. The mechanisms by which pro-resolving mediators (PRM) act in endometriosis are still little explored. Thus, this integrative review aims to synthesize the available content regarding the role of PRM in endometriosis. Experimental and in vitro studies with Lipoxin A4 demonstrate a potential inhibitory effect on endometrial lesions’ progression, attenuating pro-inflammatory and angiogenic signals, inhibiting proliferative and invasive action suppressing intracellular signaling induced by cytokines and estradiol, mainly through the FPR2/ALX. Investigations with Resolvin D1 demonstrated the inhibition of endometrial lesions and decreased pro-inflammatory factors. Annexin A1 is expressed in the endometrium and is specifically present in women with endometriosis, although the available studies are still inconsistent. Thus, we believe there is a gap in knowledge regarding the PRM pathways in patients with endometriosis. It is important to note that these substances’ therapeutic potential is evident since the immune and abnormal inflammatory responses play an essential role in endometriosis development and progression.


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