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弓形虫诱导小鼠血清睾酮变化的直接证据。

Direct evidence of Toxoplasma-induced changes in serum testosterone in mice.

机构信息

Department of Philosophy and History of Science, Faculty of Science, Charles University in Prague, Viničná 7, CZ-128 44 Prague 2, Czech Republic.

出版信息

Exp Parasitol. 2011 Jul;128(3):181-3. doi: 10.1016/j.exppara.2011.03.014. Epub 2011 Mar 31.

Abstract

Latent toxoplasmosis is known to influence the morphology of infected persons and also increases the probability of the birth of male offspring in both humans and mice. All these traits can be related to the observed differences in the concentration of testosterone between Toxoplasma-infected and Toxoplasma-free subjects. However, it is not possible to decide, using the Toxoplasma-human model, whether toxoplasmosis influences the level of testosterone in the infected host or whether individuals with different levels of testosterone vary in the probability of toxoplasma infection. Here we studied changes in the testosterone levels in the latent phase of toxoplasmosis in laboratory mice artificially infected with cystogenic but relatively virulent strain T38 of T. gondii. We observed decreased testosterone levels in both female and male mice with latent toxoplasmosis in comparison to uninfected controls (P=0.001). The present results indicate that Toxoplasma infection changes the concentration of serum testosterone in mice and human rather than changed concentration of testosterone influences the probability of the Toxoplasma infection. It is possible that the decrease of testosterone is an adaptive mechanism of infected mice aimed to compensate toxoplasmosis-induced immunosuppression observed during latent Toxoplasma infection.

摘要

潜伏性弓形体病已知会影响感染者的形态,并且还会增加人类和小鼠中雄性后代出生的概率。所有这些特征都可以与感染弓形体病和未感染弓形体病的受试者之间观察到的睾丸酮浓度差异相关。然而,使用弓形虫-人类模型,无法确定弓形体病是否会影响感染宿主的睾丸酮水平,或者睾丸酮水平不同的个体在感染弓形虫的概率上是否存在差异。在这里,我们研究了实验室感染致囊型但相对毒力的 T. gondii T38 株的潜伏性弓形体病小鼠在潜伏期睾丸酮水平的变化。与未感染对照相比,患有潜伏性弓形体病的雌性和雄性小鼠的睾丸酮水平均降低(P=0.001)。目前的结果表明,弓形体感染改变了小鼠和人类血清睾丸酮的浓度,而不是改变的睾丸酮浓度影响了弓形体感染的概率。睾丸酮的降低可能是感染小鼠的一种适应性机制,旨在补偿潜伏性弓形体感染期间观察到的弓形体病引起的免疫抑制。

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