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Hypothyroidism impairs the host immune response during the acute phase of Chagas disease
Immunobiology ( IF 2.5 ) Pub Date : 2020-11-04 , DOI: 10.1016/j.imbio.2020.152024
Pedro Alexandre Sampaio 1 , Amanda Goulart 1 , Vânia Brazão 1 , Naira Ferreira Anchieta 1 , Maiara Voltarelli Providello 1 , Gisele Bulhões Portapilla 1 , Andressa Duarte 1 , Jefferson Luiz da Silva 1 , José Clóvis do Prado Júnior 1
Affiliation  

Diseases associated with thyroid hypofunction have been the subject of studies in infectious models, since several authors have demonstrated a pivotal role of iodinated hormones (thyroxine and triiodothyronine) in the modulation of immune effector responses. Using a model of hypothyroidism induced by anti-thyroid drug, we investigated the influence of hypothyroidism in the course of acute Trypanosoma cruzi infection. For this, male Hannover Wistar rats were challenged with methimazole for 21 days (0.02% in drinking water), and water for control counterparts. After confirmation of the hypothyroidism, rats were intraperitoneally challenged with 1x105 blood trypomastigotes of the Y strain of T. cruzi. Our findings suggest that hypothyroidism impairs animal weight gain, but does not affect the health of essential organs. Interestingly, infected hypothyroid animals had a significant increase in thymic cell death, with consequent drop in lymphocyte frequency in whole blood (evaluated on the 11th day of infection). Analyzing the percentage of immune cells in the spleen, we found a strong influence of hypothyroidism as a negative regulator of B cells, and antigenic ability of macrophages (RT1b expression) in the course of the experimental chagasic infection. Enhanced serum IL-17A concentration was induced by T. cruzi infection, but hypothyroidism impaired the production of this mediator as seen in infected hypothyroid animals. Taken together, our work suggests for the first time that hypothyroidism may adversely interfere with the modulation of effective immunity in the early phase of Chagas' disease.



中文翻译:

甲减在恰加斯病急性期损害宿主免疫反应

与甲状腺功能减退相关的疾病一直是感染模型研究的主题,因为一些作者已经证明了碘化激素(甲状腺素和三碘甲状腺原氨酸)在调节免疫效应反应中的关键作用。我们使用抗甲状腺药物诱导的甲状腺功能减退模型,研究了急性克氏锥虫感染过程中甲状腺功能减退的影响。为此,雄性汉诺威 Wistar 大鼠接受了 21 天的甲巯咪唑(饮用水中的 0.02%)和对照组的水攻击。确认甲状腺功能减退后,用 1x10 5 个T. cruzi Y 品系的血锥鞭毛体对大鼠进行腹膜内攻击. 我们的研究结果表明,甲状腺功能减退症会损害动物的体重增加,但不会影响重要器官的健康。有趣的是,受感染的甲状腺功能减退动物的胸腺细胞死亡显着增加,随之而来的是全血中淋巴细胞频率的下降(在感染的第 11 天进行评估)。分析脾脏中免疫细胞的百分比,我们发现甲状腺功能减退症作为 B 细胞的负调节剂和巨噬细胞的抗原能力(RT1b 表达)在实验性恰加斯菌感染过程中具有很强的影响。T. cruzi诱导血清 IL-17A 浓度升高感染,但甲状腺功能减退会损害这种介质的产生,如在受感染的甲状腺功能减退动物中所见。总之,我们的工作首次表明,甲状腺功能减退症可能会对恰加斯病早期有效免疫的调节产生不利影响。

更新日期:2020-11-21
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