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碘缺乏会诱发Wistar大鼠的甲状腺自身免疫反应。

Iodine deficiency induces thyroid autoimmune reactivity in Wistar rats.

作者信息

Mooij P, de Wit H J, Bloot A M, Wilders-Truschnig M M, Drexhage H A

机构信息

Department of Immunology, Erasmus University, Rotterdam, The Netherlands.

出版信息

Endocrinology. 1993 Sep;133(3):1197-204. doi: 10.1210/endo.133.3.8103449.

Abstract

The last 2 decades it has become clear that iodine deficiency has a modulating effect on the thyroid autoimmune response in humans. Also, in animals that spontaneously develop autoimmune thyroid disease, evidence is accumulating that a low iodine intake can modulate thyroid autoimmune reactivity. However, it is still not clear what the effect of a low iodine intake on thyroid autoimmune reactivity is in normal nonautoimmune animals. To study the relationship of a dietary low iodine intake on the thyroid autoimmune reactivity in nonautoimmune animals, normal Wistar rats (female) were kept on an enriched iodine diet (daily iodine intake of 100 micrograms iodine), a "for our area normal" (conventional) diet (COD; daily iodine intake of 7 micrograms iodine), a low iodine diet (LID; 2 days of 1% KCLO4, followed by iodine-deficient drinking water/pellets), or an extremely low iodine diet (LID+; 1% KCLO4 continuously in the drinking water and iodine-deficient pellets). The enriched iodine diet rats were euthyroid (T3, approximately 8 nM/liter: T4, approximately 50 nM/liter; TSH, approximately 2 ng/ml), had a normal thyroid weight (approximately 12.5 mg), and showed only minimal signs of local thyroid immune reactivity; low numbers of intrathyroidal dendritic cells (DC; approximately 35 DC/mm2), CD4+ cells (approximately 2 cells/mm2), and CD8+ cells (approximately 2.5 cells/mm2) were found in combination with low anticolloid antibody production (incidence of positive animals, 12.5%). The COD resulted in a normal thyroid function. The rats were euthyroid (range of T3, 1.6-1.2 nM/liter; T4, approximately 50 nM/liter; TSH, approximately 2 ng/ml) and had a normal thyroid weight (approximately 12.5 mg). However, some signs of thyroid autoimmune reactivity were found [number of intrathyroidal DC, approximately 40/mm2; approximately 3 CD4-positive (CD+) cells/mm2; approximately 3 CD8+ cells/mm2; together with a 30% incidence of anticolloid antibodies]. The LID and LID+ not only induced goiter formation [thyroid weight, 27.3 +/- 4.2 mg (mean +/- SD) after 12 weeks of LID and 38.4 +/- 5.3 mg after 4 weeks of LID+] and low production of T4 by the thyroid [28 +/- 3 nM/liter (mean +/- SD)] after 12 weeks of LID and 14 +/- 3 nM/liter after 2 weeks of LID+], but also induced various signs of thyroid autoimmune reactivity.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

在过去20年里,已经明确碘缺乏对人类甲状腺自身免疫反应具有调节作用。此外,在自发发生自身免疫性甲状腺疾病的动物中,越来越多的证据表明低碘摄入可调节甲状腺自身免疫反应性。然而,低碘摄入对正常非自身免疫动物的甲状腺自身免疫反应性有何影响仍不清楚。为了研究饮食中低碘摄入与非自身免疫动物甲状腺自身免疫反应性的关系,将正常Wistar大鼠(雌性)分别置于高碘饮食(每日碘摄入量为100微克碘)、“本地区正常”(传统)饮食(COD;每日碘摄入量为7微克碘)、低碘饮食(LID;2天给予1%高氯酸钾,随后给予缺碘饮用水/颗粒饲料)或极低碘饮食(LID+;饮用水中持续添加1%高氯酸钾和缺碘颗粒饲料)中饲养。高碘饮食组大鼠甲状腺功能正常(T3约8纳摩尔/升;T4约50纳摩尔/升;TSH约2纳克/毫升),甲状腺重量正常(约12.5毫克),仅表现出轻微的局部甲状腺免疫反应迹象;甲状腺内树突状细胞(DC;约35个DC/平方毫米)、CD4+细胞(约2个细胞/平方毫米)和CD8+细胞(约2.5个细胞/平方毫米)数量较少,同时抗甲状腺球蛋白抗体产生水平较低(阳性动物发生率为12.5%)。COD组大鼠甲状腺功能正常。大鼠甲状腺功能正常(T3范围为1.6 - 1.2纳摩尔/升;T4约50纳摩尔/升;TSH约2纳克/毫升),甲状腺重量正常(约12.5毫克)。然而,发现了一些甲状腺自身免疫反应的迹象[甲状腺内DC数量约40/平方毫米;约3个CD4阳性(CD+)细胞/平方毫米;约3个CD8+细胞/平方毫米;抗甲状腺球蛋白抗体发生率为30%]。LID和LID+不仅诱导甲状腺肿大形成[LID喂养12周后甲状腺重量为27.3±4.2毫克(平均值±标准差),LID+喂养4周后为38.4±5.3毫克],且LID喂养12周后甲状腺T4分泌减少[28±3纳摩尔/升(平均值±标准差)],LID+喂养2周后为14±3纳摩尔/升,还诱导了各种甲状腺自身免疫反应的迹象。(摘要截选至400字)

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