CHRONIC CENTRAL-NERVOUS-SYSTEM EXPOSURE TO INTERLEUKIN-1-BETA CAUSES CATABOLISM IN THE RAT

Interleukin-1 (IL-1) and interleukin-6 (IL-6) are thought to play a ro le in mediating weight loss, net protein catabolism, anorexia, and fev er after infection or injury. Because IL-1 and IL-6 can be synthesized in the brain and have been shown to be increased in central nervous s ystem (CNS) infections, we investigated the metabolic consequences of prolonged CNS exposure to these cytokines. At equivalent doses, intrac erebroventricular infusion of IL-1, but not IL-6, caused negative nitr ogen balance, weight loss, and anorexia. Intracerebroventricular infus ion of IL-1 also caused adrenocortical activation, as indicated by inc reased adrenal weight and plasma corticosterone, and decreased thymus weight. However, clamping plasma glucocorticoids at low levels by adre nalectomy and corticosterone pellet replacement did not attenuate IL-1 -induced losses of body weight and nitrogen. We conclude that centrall y produced IL-1 could play an important role in the metabolic alterati ons associated with CNS injury or infection and that these effects may not be solely attributable to increased secretion of glucocorticoids.