Reciprocal Relationships Between the Immune and Central Nervous System
Abstract
We are investigating how the neuroendocrine system affects macrophage activation and how products derived from activated macrophages affect animal behavior. We have shown that interferon-lambda effectively counteracts the suppression in the synthesis of macrophage-derived tumor necrosis factors-alpha caused by both glucocorticoids and transforming growth factor beta-2. Furthermore, the decline in synthesis of TNF-a and secretion of superoxide anion that occurs in macrophages from aged rats can be significantly reversed by syngeneic pituitary grafts. Macrophage productas are also responsible for some aspects of sickness behavior, as defined by peripheral and central injections of interleukin-1 inducing conditioned taste aversion in both endotoxin sensitive and resistant mice. Indomethacin and aspirin do not block the effects of IL-1 on conditioned taste aversion, but they both inhibit the reductions in social exploration and schedule-controlled behavior of rats injected peripherally with IL-1. These data support the idea that macrophage products are responsible for behavioral symptoms of illness following a bacterial infection, and that macrophage activation is regulated by hormones from the pituitary gland. Macrophage, IL-1, Transforming growth factor B2, Corticosteroids, IFN-y, Conditioned taste aversion, Schedule-controlled behavior, Prostaglandins, Biochemistry, Physiology
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 1990
- Accession Number
- ADA221259
Entities
People
- Keith W. Kelley
- Robert Dantzer
Organizations
- University of Illinois Urbana–Champaign