Effects of Acute Stress or Centrally Injected Interleukin-1β on Neuropeptide Expression in the Immune System

Abstract

Acute stress stimulates the expression and release of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) from the hypothalamus, and the pro-opiomelanocortin products P-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)-lβ 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-lβ increased contents of CRH, AVP, ACTH and P-endorphin in the spleens of both sham-operated and adrenalectomised (ADX) rats. IL-lβ 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-ip on neuropeptide expression in the spleen are independent of glucocorticoids, whereas IL-lβ stimulation of neuropeptide expression in the thymus is dependent on circulating glucocorticoids. There were significant correlations between increases in CRH, ACTH and β-endorphin in the spleen, and between CRH and ACTH in the thymus, consistent with the suggestion that IL-lβ-induced increases in ACTH and β-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.