A link exists between immune function and psychiatric conditions, particularly depressive and anxiety disorders. Psychological stress is a powerful trigger for these disorders and stress influences immune state. However, the nature of peripheral immune changes after stress conflicts across studies, perhaps due to the focus on few measures of pro-inflammatory or anti-inflammatory processes. The basolateral amygdala (BLA) is critical for emotion, and plays an important role in the effects of stress on anxiety. As such, it may be a primary central nervous system (CNS) mediator for the effects of peripheral immune changes on anxiety after stress. Therefore, this study aimed to delineate the influence of stress on peripheral pro-inflammatory and anti-inflammatory aspects, BLA immune activation, and its impact on BLA neuron activity. To produce a more encompassing view of peripheral immune changes, this study used a less restrictive approach to categorize and group peripheral immune changes. We found that repeated social defeat stress in adult male Sprague-Dawley rats increased the frequencies of mature T-cells positive for intracellular type 2-like cytokine and serum pro-inflammatory cytokines. Principal component analysis and hierarchical clustering was used to guide grouping of T-cells and cytokines, producing unique profiles. Stress shifted the balance towards a specific set that included mostly type 2-like T-cells and pro-inflammatory cytokines. Within the CNS component, repeated stress caused an increase of activated microglia in the BLA, increased anxiety-like behaviors across several assays, and increased BLA neuronal firing in vivo that was prevented by blockade of microglia activation. Because repeated stress can trigger anxiety states by actions in the BLA, and altered immune function can trigger anxiety, these results suggest that repeated stress may trigger anxiety-like behaviors by inducing a pro-inflammatory state in the periphery and the BLA. These results begin to uncover how stress may recruit the immune system to alter the function of brain regions critical to emotion.

中文翻译：

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重复压力会诱发促炎状态，增加杏仁核神经元和小胶质细胞的激活，并引起成年雄性大鼠的焦虑

免疫功能与精神疾病，尤其是抑郁症和焦虑症之间存在联系。心理压力是这些疾病的强大触发因素，压力会影响免疫状态。然而，跨研究的压力冲突后外周免疫变化的性质，可能是由于关注促炎或抗炎过程的几个措施。基底外侧杏仁核 (BLA) 对情绪至关重要，在压力对焦虑的影响中起着重要作用。因此，它可能是外周免疫变化对压力后焦虑的影响的主要中枢神经系统 (CNS) 介质。因此，本研究旨在描绘压力对外周促炎和抗炎方面的影响、BLA 免疫激活及其对 BLA 神经元活动的影响。为了对外周免疫变化产生更全面的看法，本研究使用了一种限制较少的方法来对外周免疫变化进行分类和分组。我们发现成年雄性 Sprague-Dawley 大鼠的反复社交失败压力增加了细胞内 2 型细胞因子和血清促炎细胞因子呈阳性的成熟 T 细胞的频率。主成分分析和层次聚类用于指导 T 细胞和细胞因子的分组，产生独特的特征。压力将平衡转向特定的一组，其中主要包括 2 型 T 细胞和促炎细胞因子。在 CNS 组件中，反复压力导致 BLA 中激活的小胶质细胞增加，在多项检测中增加了类似焦虑的行为，和增加体内 BLA 神经元放电，这是通过阻断小胶质细胞激活来阻止的。因为反复压力可以通过 BLA 中的动作触发焦虑状态，而改变的免疫功能可以触发焦虑，这些结果表明反复压力可能通过诱导外周和 BLA 的促炎状态来触发焦虑样行为。这些结果开始揭示压力如何招募免疫系统来改变对情绪至关重要的大脑区域的功能。