Effects of chronic psychosocial stress on the systemic immune status

根据暴露时间的长短，心理社会压力对免疫系统有相反的影响。一些啮齿类动物的研究表明，急性应激增强了免疫细胞的活性，而慢性应激被认为主要是抑制免疫功能。然而，一些动物模型和人类研究表明，慢性应激与局部炎症的相关性表明，这种模式应该重新评估。糖皮质激素（GC）在应激源暴露时释放，是发挥抗炎作用的重要介质。因此，有利于循环GC减少或免疫细胞GC抗性发展的条件与激活的免疫状态有关。在慢性从属菌落（CSC）收容期间，GC血浆水平仅在最初48小时内短暂升高，并在a /ards后恢复到基线水平。发展中的肾上腺功能不全似乎进一步促进应激小鼠的低皮质。巧合的是，观察到自发性局部肠道炎症加剧。与此相对应，我们提出CSC也促进免疫细胞的全身活化。因此，我们计划表征小鼠在CSC过程中的免疫状态，以揭示系统性免疫细胞区室改变的细胞和分子机制，并评估慢性应激暴露对抗微生物防御机制的影响。

Depending on the duration of exposure psychosocial stress has opposing effects on the immune system. Several studies in rodents demonstrated that acute stress enhances the immune celt aciivity, whereas chronic stress has been considered mainly to suppress immune funclions. However, some animat models and studies in humans correlafing chronic stress with local inflammations indicate that this paradigm should be re-evaluated. Glucocorticoids (GC) are released in response to exposure lo stressors and are important mediators exerting an anti-inflammatory effect. Conditions favoring either a reduciion of circulating GC or the devetopment of GC resistance of immune cells are therefore associated with an activated immune status. During chronic subordinate colony (CSC) housing, GC plasma levels are only transiently elevated during the first 48h and return to baseline levels aftenA/ards. The developing adrenal insufficiency seems to further promote hypocorticism in stressed mice. By coincidence, the exacerbation of spontaneous local gut infiammafion was observed. Corresponding to that, we propose that CSC also promotes systemic activation of immune celts. Thus, we plan to characterise the immune status of mice in the course of CSC to reveal the cellular and molecular mechanisms underlying alterafions of the systemic immune cell compartment, and to assess the consequences of chronic stress exposure on anli-microbiat defense mechanisms.