Chemical sympathectomy alters cytotoxic T lymphocyte responses to herpes simplex virus infection.

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.