Cachectin/Tumor Necrosis Factor and the Pituitary-Adrenal Axis
Abstract
Results from our studies investigating immune-neuroendocrine interactions have yielded interesting and novel findings. In unanesthetized rats, TNF (10ug/kg) was a potent stimulus for ACTH release without affecting hemodynamics. In vitro, TNF was without effect on the basal secretion of corticosterone (CS) but inhibited ACTH-stimulated CS release. Likewise, TNF inhibited TSH-stimulated thyroglobulin release from cultured human thyroid cells. In vitro, ACTH tended to inhibit LPS-induced TNF release from cultured macrophages, however, in the presence of serum-free media, ACTH appeared to potentiate TNF release. Also, the dose-response curves for CS and dexamethasone (inhibitors of TNF release) were shifted to the right. Together these findings suggest that factors present in sera and absent in serum-free media may interfere with LPS binding and/or uptake into macrophages. Results from these studies have provided additional knowledge and insight into the bidirectional communication between the neuroendocrine and immune systems. Keywords: Tumor necrosis factors; Cachectin; ACTH; Corticosterone thyroglobulin; Macrophage; LPS; Dexamethasone; cAMP; Cyclic adenosine monophosphate; Monokines; Cytokines.
Document Details
- Document Type
- Technical Report
- Publication Date
- Feb 28, 1990
- Accession Number
- ADA218837
Entities
People
- Diana S. Malcolm
Organizations
- Uniformed Services University of the Health Sciences