A pre-conditioning stress accelerates increases in mouse plasma inflammatory cytokines induced by stress.
A pre-conditioning stress accelerates increases in mouse plasma inflammatory cytokines induced by stress.
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DOI：
10.1186/s12868-015-0169-z
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发表时间：
2015-05-07
期刊：
影响因子：
2.4
通讯作者：
Beurel E
中科院分区：
文献类型：
--
作者：
Cheng Y;Jope RS;Beurel E
重度抑郁症是一种流行病，目前可用的干预措施治疗不足。压力增加了患者和啮齿动物模型对抑郁症的易感性。抑郁症还与炎症的异常激活相关，例如白细胞介素（IL）-1β、IL-6和肿瘤坏死因子-α（TNFα）的循环水平升高。本研究的两个主要目标是（i）确定细胞因子的变化，测量广泛的19种细胞因子，和（ii）测试预处理应激是否改变了对后续应激的炎症反应。压力诱导的小鼠血浆细胞因子的变化进行了测量，通过多重管理后，每天一次或两次的压力，不可避免的脚电击使用习得性无助的范例建模抑郁样行为。不可避免的足部电击增加了IL-1β、IL-6、TNFα、IL-3、IL-10、IL-13、IL-17 A、IL-5、GM-CSF、IL-12（p70）、IFN-γ、MIP-1α、MIP-1β、IL-1α、IL-2、KC、RANTES和G-CSF的血浆水平，峰值水平出现在应激后6 - 12小时。预处理的小鼠24小时前与一个等效的不可避免的脚休克应力导致类似的幅度的增加，在大多数细胞因子发生后，一个单一的压力，但加速增加，导致大多数细胞因子的水平达到峰值后1小时的压力。这些结果表明，一个单一的压力诱导许多细胞因子的表达，和连续的，每天的压力加速细胞因子的产生速度。急性应激广泛激活小鼠的炎症，并且在反复应激后炎症反应更快，这些行为可能导致应激对抑郁症和其他应激相关疾病的有害影响。
Major depressive disorder is a prevalent disease that is inadequately treated with currently available interventions. Stress increases susceptibility to depression in patients and rodent models. Depression is also associated with aberrant activation of inflammation, such as increases in circulating levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNFα). The two main goals of this study were (i) to identify cytokine changes measuring a broad panel of 19 cytokines, and (ii) to test if a pre-conditioning stress altered the inflammatory response to a subsequent stress. Stress-induced changes in mouse plasma cytokines were measured by multiplex following administration of one or two daily stresses of inescapable foot shocks using the learned helplessness paradigm for modeling depression-like behavior. Administration of inescapable foot shocks increased plasma levels of IL-1β, IL-6, TNFα, IL-3, IL-10, IL-13, IL-17A, IL-5, GM-CSF, IL-12(p70), IFN-γ, MIP-1α, MIP-1β, IL-1α, IL-2, KC, RANTES and G-CSF, with peak levels occurring in the range of 6 to 12 hr after stress. Pre-conditioning the mice 24 hr before with an equivalent inescapable foot shock stress resulted in similar magnitudes of increases in most cytokines as occurred after a single stress, but accelerated the increase, causing the levels of most cytokines to peak 1 hr after stress. These results demonstrate that a single stress induces the expression of many cytokines, and that sequential, daily stresses accelerates the rate of cytokine production. Acute stress broadly activates inflammation in mice, and the inflammatory response is more rapid following repeated stress, actions that may contribute to deleterious effects of stress on depression and other stress-linked diseases.
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