کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
923176 | 921072 | 2007 | 11 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Thymus atrophy during Trypanosoma cruzi infection is caused by an immuno-endocrine imbalance Thymus atrophy during Trypanosoma cruzi infection is caused by an immuno-endocrine imbalance](/preview/png/923176.png)
C57BL/6 mice infected with Trypanosoma cruzi, the causal agent of Chagas’ disease, develop severe thymocyte depletion paralleled by an inflammatory syndrome mediated by tumor necrosis factor-alpha (TNF-α). The exacerbated inflammatory reaction induces the activation of hypothalamus–pituitary–adrenal (HPA) axis with the consequent release of corticosterone (CT) into the circulation as a protective response. Thymocyte apoptosis has been related to a rise in TNF-α and CT levels, and both mediators are increased in T. cruzi-infected C57BL/6 mice. The depletion of immature CD4+CD8+ thymocytes by apoptosis following infection with the parasite was still present in mice defective in both types of TNF-receptors (double knockout). However, thymic atrophy was prevented by adrenalectomy combined with RU486 administration, demonstrating that this is a CT-driven phenomenon. Our results put emphasis on the importance of an appropriated immuno-endocrine balance during T. cruzi infection and show that functional deviations in the immuno-endocrine equilibrium have profound effects on the thymus and disease outcome.
Journal: Brain, Behavior, and Immunity - Volume 21, Issue 7, October 2007, Pages 890–900