Interleukin-1b-induced fever in young and old Long–Evans rats

ated with a blunted or absent fever response to naturally occurring infections or to the peripheral administration of bacterial products and proinflammatory cytokines, including interleukin-1b (IL-1b). Whether old rats also exhibit an attenuated fever response when challenged with direct brain administration of IL-1b is unknown. Here we investigated the fever response of young (3–5 mo) and old (24–26 mo) Long-Evans rats to the intracerebroventricular microinfusion of IL-1b. Core body temperature was monitored by telemetry in freely moving rats. Intracerebroventricularly adminis-tered IL-1b induced comparable increases in body tempera-ture in young and old Long-Evans rats. In the two groups, IL-1b-induced fever was similar both in latency to peak fever and maximal fever response, whether the cytokine was administered 2 h after lights on or just before lights off. These data show that old Long-Evans rats are not defective in their capacity to develop a fever in response to brain administra-tion of IL-1b. cytokine; intracerebroventricular; aging; core temperature; nervous system; immune system INTERLEUKIN (IL)-1b is a proinflammatory cytokine that induces fever (2, 11, 14). In rodents, when IL-1b is administered intracerebroventricularly, low-nanogram doses are sufficient to induce fever. When IL-1b is administered peripherally, microgram doses are re-quired to induce equivalent fevers. This suggests that the pyrogenic effects induced by low doses of centrally administered IL-1b are due to its direct action in the central nervous system (CNS). Aging is associated with alterations in the host physiological responses to inflammatory and infectious stimuli (4). Often, elderly patients show a blunted fever or no fever at all in response to infection (18). The same is true in old rodents: peripheral (intraperitoneal, intravenous) administration of bacterial products o