In the central nervous system in vivo interleukin-1b leads to cerebral spinal fluid lymphocytosis but not fever

Introduction: In the periphery, IL-1ß has well-recognized roles in initiating & perpetuating inflammatory cellular responses & in producing fever. Clinically, fever is often the first objective sign of systemic illness. in the CNS. the effects of lL-1 on an intact mammalian level is uncertain. In this study, following intracerebroventricular (I.c.v.) administration, we examined the effect of IL-1 on cerebrospinai fluid (CSF) white blood cell count (WBC) & fever. Methods: Dogs (n=8) were each surgically prepared with an indweUing I.C.V. catheter system. After at least one month of recovery, human IL-1 was given i.c.v. in doses of 50,100 & 200 ng/kg. Controls received 0.1% BSA in normal saline. Blood & CSF specimens were obtained before & for 3 hours after dosing. Body temperature was measured continuously throughout. Biofluid analyses used manual & automated methods. Results: The findings demonstrated a rapid increase in CSF leukocyte count. By 10 min. after administration, peak cell counts were obtained. For the 100 & 200 ng/kg groups, the WBCs were 36 ±8.7 mm3(Mean ± SEM) & 102 ±28.2 mm3, respectively. These resufts were significantly different from control (p< 0.05, t-test). Following, these levels gradually decreased back to baselne except at the highest dose which were persistently elevated. Throughout, the white cans were predominately mononudear. Body temperature did not significantly increase from baseline. Conclusion: Following the Lev. administration in dogs, IL-1 leads to a dose-dependent mononudear CSF leukocytosis. These findings suggest that disorders that lead to a predominantly CSF monocytosis (such as aseptic meningitis) may be mediated by IL-1. Furthermore, at higher concentrations, there may be a contribution by endogenous IL-1 or other cytokines may be involved. In addition, it appears that fever requires a higher level of this cytokine or possibly another mechanism is involved.