Intravenous granulocyte colony-stimulating factor increases the release oftumour necrosis factor and interleukin-1 beta into the cerebrospinal fluid, but does not inhibit the growth of Streptococcus pneumoniae in experimental meningitis

Granulocyte colony-stimulating factor (G-CSF) possesses an antimicrobial ef fect in several animal models of infection. To evaluate a possible effect o f G-CSF on the course of pneumococcal meningitis, rabbits infected intracis ternally (i.c.) with Streptococcus pneumoniae type 3 (n = 7) received 50 mu g/kg of rhG-CSF intravenously (i.v.) 1 h prior to infection. Seven infecte d animals served as controls. Uninfected rabbits received 10 mu g of G-CSF (n = 3), 2 mu g G-CSF (n = 3) or saline (n = 3) i.c. G-CSF injected i.c. di d not produce cerebrospinal fluid (CSF) leucocytosis. Compared with the con trol group, i.v. G-CSF given prior to i.c. infection increased the percenta ge of granulocytes in blood 6 h and 12 h after infection. Twelve hours afte r infection, CSF tumour necrosis factor (TNF) activity and CSF interleukin (IL)-1 beta concentrations were significantly higher in G-CSF-treated anima ls. G-CSF did not decrease bacterial growth in the subarachnoid space and t he CSF leucocyte densities were not influenced. At 24 h after infection, G- CSF did not reduce the CSF concentrations of neurone-specific enolase and t he density of apoptotic neurones in the dentate gyrus of the hippocampus. I n conclusion, i.v. G-CSF increased the concentration of pro-inflammatory cy tokines in the CSF but did not decrease the growth of Streptococcus pneumon iae in the subarachnoid space.