Leo N A, Bonneau R H
Department of Microbiology and Immunology and Program in Neuroscience, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA.
Ann N Y Acad Sci. 2000;917:923-34. doi: 10.1111/j.1749-6632.2000.tb05458.x.
Numerous studies have sought to delineate the impact of neuroendocrine function on overall immune responsiveness. Using various murine models, we and others have previously shown that both adrenal-dependent and adrenal-independent mechanisms regulate components of the primary and memory cellular immune responses to herpes simplex virus type 1 (HSV-1) infection. We have extended these studies by determining the impact of 6-hydroxydopamine (6-OHDA)-induced peripheral sympathetic denervation on these responses. C57BL/6 mice treated with 6-OHDA (200 mg/kg) were inhibited in their ability to generate primary, HSV-specific cytotoxic T lymphocytes (CTL) in response to HSV infection. Sympathectomy also suppressed the activation and function of HSV-specific memory CTL (CTLm). In addition, administration of 6-OHDA resulted in a transient but substantial increase in levels of circulating corticosterone and hypothalamic Fos expression. Together, these findings suggest that peripheral sympathetic denervation may modulate immune function via activation of the hypothalamic-pituitary-adrenal (HPA) axis.
众多研究试图阐明神经内分泌功能对整体免疫反应性的影响。利用各种小鼠模型，我们和其他研究人员先前已表明，肾上腺依赖和肾上腺非依赖机制均调节对1型单纯疱疹病毒（HSV-1）感染的原发性和记忆性细胞免疫反应的组成部分。我们通过确定6-羟基多巴胺（6-OHDA）诱导的外周交感神经去神经支配对这些反应的影响，扩展了这些研究。用6-OHDA（200mg/kg）处理的C57BL/6小鼠对HSV感染产生原发性HSV特异性细胞毒性T淋巴细胞（CTL）的能力受到抑制。交感神经切除术还抑制了HSV特异性记忆CTL（CTLm）的激活和功能。此外，给予6-OHDA导致循环皮质酮水平和下丘脑Fos表达短暂但显著增加。这些发现共同表明，外周交感神经去神经支配可能通过激活下丘脑-垂体-肾上腺（HPA）轴来调节免疫功能。
