Effects of Acute Stress or Centrally Injected Interleukin-1beta on Neuropeptide Expression in the Immune System.
Effects of Acute Stress or Centrally Injected Interleukin-1beta on Neuropeptide Expression in the Immune System.
复制标题
急性应激或集中注射白细胞介素 1β 对免疫系统中神经肽表达的影响。
作者：
D. S. Jessop;J. A. Douthwaite;G. L. Condé;S. Lightman;Colin M. Dayan;M. Harbuz
急性应激刺激促肾上腺皮质激素释放激素（CRH）和精氨酸加压素（AVP）从下丘脑的表达和释放，以及阿黑皮素原产物β-内啡肽和ACTH从垂体前叶的表达和释放。这些神经肽也在免疫组织中表达，并且已经提出它们可以通过旁分泌机制调节对应激的免疫应答。我们对大鼠进行束缚应激或中枢注射白细胞介素（IL）-1 β，以确定这些急性刺激是否可以改变脾脏和胸腺中神经肽的表达。束缚应激显着增加了胸腺提取物中所有这些神经肽的含量，但没有增加脾脏提取物中所有这些神经肽的含量。侧脑室注射IL-1 β可增加假手术和肾上腺切除（ADX）大鼠脾脏CRH、AVP、ACTH和β-内啡肽的含量。IL-1 β增加假手术大鼠胸腺CRH和ACTH的含量，但这些增加在ADX大鼠中未观察到。这些结果表明，IL-1 β对脾脏中神经肽表达的影响是独立的糖皮质激素，而IL-1 β刺激胸腺中神经肽表达依赖于循环糖皮质激素。脾脏中CRH、ACTH和β-内啡肽的增加之间以及胸腺中CRH和ACTH之间存在显著相关性，这与IL-1 β诱导的ACTH和β-内啡肽增加可能通过CRH介导的建议一致。这些结果提供了证据表明，应激可以直接影响免疫组织中的神经肽表达。因此，压力可能会影响免疫功能，通过旁分泌机制，涉及局部合成的神经肽，以及通过激活下丘脑-垂体-肾上腺轴。
Acute stress stimulates the expression and release of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) from the hypothalamus, and the pro-opiomelanocortin products beta-endorphin and ACTH from the anterior pituitary. These neuropeptides are also expressed in immune tissues, and it has been proposed that they may modulate immune responses to stress through paracrine mechanisms. We subjected rats to restraint stress or central injection of interleukin (IL)-1beta to determine whether these acute stimuli can alter the expression of neuropeptides in the spleen and thymus. Restraint stress significantly increased the contents of all these neuropeptides in thymic, but not splenic, extracts. A single icv injection of IL-1beta increased contents of CRH, AVP, ACTH and beta-endorphin in the spleens of both sham-operated and adrenalectomised (ADX) rats. IL-1beta increased thymic contents of CRH and ACTH in sham-operated rats but these increases were not observed in ADX rats. These results suggest that the effects of IL-1beta on neuropeptide expression in the spleen are independent of glucocorticoids, whereas IL-1beta stimulation of neuropeptide expression in the thymus is dependent on circulating glucocorticoids. There were significant correlations between increases in CRH, ACTH and beta-endorphin in the spleen, and between CRH and ACTH in the thymus, consistent with the suggestion that IL-1beta-induced increases in ACTH and beta-endorphin may be mediated through CRH. These results provide evidence that stressors can directly influence neuropeptide expression in immune tissues. Thus stress may influence immune functions through paracrine mechanisms involving locally synthesised neuropeptides as well as through activation of the hypothalamo-pituitary-adrenal axis.