Bidirectional communication between the neuroendocrine stress and immune systems permits classically anti-inflammatory glucocorticoids to exert pro-inflammatory effects in specific cells and tissues. Liver macrophages/Kupffer cells play a crucial role in initiating inflammatory cascades mediated by the release of pro-inflammatory cytokines following tissue injury. However, the effects of repeated acute psychological stress on hepatic inflammatory phenotype and macrophage activation state remains poorly understood. We have utilised a model of repeated acute stress in rodents to observe the changes in hepatic inflammatory phenotype, including anti-inflammatory vitamin D status, in addition to examining markers of classically and alternatively-activated macrophages. Male Wistar rats were subjected to control conditions or 6 h of restraint stress applied for 1 or 3 days (n = 8 per group) after which plasma concentrations of stress hormone, enzymes associated with liver damage, and vitamin D status were examined, in addition to hepatic expression of pro- and anti-inflammatory markers. Stress increased glucocorticoids and active vitamin D levels in addition to expression of glucocorticoid alpha/beta receptor, whilst changes in circulating hepatic enzymes indicated sustained liver damage. A pro-inflammatory response was observed in liver tissues following stress, and inducible nitric oxide synthase being observed within hepatic macrophage/Kupffer cells. Together, this suggests that stress preferentially induces a pro-inflammatory response in the liver.

神经内分泌应激和免疫系统之间的双向通讯允许传统的抗炎糖皮质激素在特定细胞和组织中发挥促炎作用。肝脏巨噬细胞/库普弗细胞在组织损伤后释放促炎细胞因子介导的炎症级联反应中发挥着至关重要的作用。然而，反复急性心理应激对肝脏炎症表型和巨噬细胞激活状态的影响仍知之甚少。我们利用啮齿动物反复急性应激模型来观察肝脏炎症表型的变化，包括抗炎维生素 D 状态，此外还检查经典和替代激活巨噬细胞的标记物。雄性 Wistar 大鼠接受对照条件或 6 小时的束缚应激，持续 1 或 3 天（每组 n = 8），然后检查应激激素的血浆浓度、与肝损伤相关的酶以及维生素 D 状态。促炎和抗炎标记物的肝脏表达。除了糖皮质激素 α/β 受体的表达外，压力还会增加糖皮质激素和活性维生素 D 的水平，而循环肝酶的变化表明存在持续的肝损伤。在应激后的肝组织中观察到促炎症反应，并且在肝巨噬细胞/库普弗细胞内观察到诱导型一氧化氮合酶。总之，这表明压力优先诱发肝脏的促炎症反应。