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睾酮在肥胖品系(OS)鸡自发性自身免疫性甲状腺炎中的作用。

The role of testosterone in spontaneous autoimmune thyroiditis of Obese strain (OS) chickens.

作者信息

Fässler R, Dietrich H, Krömer G, Böck G, Brezinschek H P, Wick G

机构信息

Institute for General and Experimental Pathology, University of Innsbruck, Medical School, Austria.

出版信息

J Autoimmun. 1988 Feb;1(1):97-108. doi: 10.1016/0896-8411(88)90081-9.

Abstract

We have recently reported a two-fold defect in glucocorticoid mediated immunoregulation in the Obese strain (OS) of chickens with spontaneous autoimmune thyroiditis (SAT): (i) a decreased basal corticosterone (CN) tonus due to an elevation of plasma corticosteroid-binding globulin (CBG) and (ii) an impaired CN rise in response to antigenic stimuli as well as lymphokines produced after mitogenic stimulation. The aim of the present study was to investigate the pathophysiological relevance of testosterone for the development of SAT. Compared to healthy normal White Leghorn chickens (NWL) the basal sex hormone tonus as well as androgen receptors of bursal tissue are not altered in the OS. Administration of sheep red blood cells (SRBC) or lymphokine containing conditioned media not only increased CN plasma levels but concomitantly modulated testosterone serum concentrations, although in an inverse direction and without significant difference between OS and healthy control chickens. These results suggest that, in contrast to the glucocorticoid system, androgen tonus as well as its modulation by immune signals are normal in the OS. The mode of action by which androgens exert their known beneficial effect on the development of SAT was also studied. According to our findings the capacity of testosterone to prevent SAT when administered during the posthatching period can be attributed to direct effects on bursal epithelial cells as well as indirect mechanisms, namely a fall in CBG levels leading to normalization of the CN tonus.

摘要

我们最近报道,患有自发性自身免疫性甲状腺炎(SAT)的肥胖品系(OS)鸡在糖皮质激素介导的免疫调节方面存在双重缺陷:(i)由于血浆皮质类固醇结合球蛋白(CBG)升高,基础皮质酮(CN)张力降低;(ii)对抗抗原刺激以及有丝分裂原刺激后产生的淋巴因子时,CN升高受损。本研究的目的是探讨睾酮在SAT发病中的病理生理相关性。与健康的正常白来航鸡(NWL)相比,OS鸡的基础性激素张力以及法氏囊组织的雄激素受体没有改变。给予绵羊红细胞(SRBC)或含淋巴因子的条件培养基不仅会提高血浆CN水平,还会同时调节血清睾酮浓度,尽管方向相反,且OS鸡与健康对照鸡之间无显著差异。这些结果表明,与糖皮质激素系统不同,OS鸡的雄激素张力及其受免疫信号的调节是正常的。我们还研究了雄激素对SAT发病产生已知有益作用的作用方式。根据我们的研究结果,孵化后时期给予睾酮预防SAT的能力可归因于对法氏囊上皮细胞的直接作用以及间接机制,即CBG水平下降导致CN张力正常化。

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