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.
