Search

We have developed an extraction method and radioimmunoassay for the measurement of interleukin-1 beta (IL-1 beta) in rat tissues, using an antibody specific for IL-1 beta, IL-1 beta was detected in the spleen and thymus of control rats. Adrenalectomy (ADX) had no effect upon control levels of IL-1 beta. In animals with adjuvant-induced arthritis, IL-1 beta content in the spleen and thymus increased after 14 days. These increases in tissue IL-1 beta contents were not evident in ADX arthritic animals. We conclude that IL-1 beta synthesis is stimulated in tissues of the immune system following the development of adjuvant-induced arthritis. Failure to observe elevated levels of tissue IL-1 beta in ADX arthritic rats may be evidence for tissue depletion due to increased IL-1 beta release in the absence of circulating corticosteroids.

The role of catecholamines in regulating the neuroendocrine stress response is controversial. We have investigated the effects of unilateral ventral noradrenergic bundle (VNAB) lesions on corticotrophin-releasing factor (CRF) and proenkephalin A mRNA responses in the parvocellular paraventricular nucleus (pPVN) to both physical and psychological stresses. We have also determined the effects of direct bilateral PVN lesions on CRF mRNA, plasma ACTH and corticosterone responses to psychological stress. 6-OHDA lesions whether to the VNAB or direct to the PVN did not result in any change in basal levels of CRF mRNA. Depletion of endogenous noradrenaline following unilateral lesions of the VNAB did not affect the CRF mRNA or the proenkephalin A mRNA response to stress. These data suggest that noradrenergic pathways are not involved in maintaining basal levels of CRF mRNA and that the noradrenergic input through the VNAB does not mediate the accumulation of CRF and proenkephalin A mRNAs in response to these stressors. Direct bilateral lesions to the PVN prevented the accumulation of CRF mRNA but not the ACTH and corticosterone responses to restraint stress. This suggests that monoamines are involved in the regulation of CRF mRNA through a mechanism independent of CRF-41 secretion.