Subarachnoid hemorrhage (SAH) elicits an inflammatory response in the 
subarachnoid space, which is mediated by the release of various cytokines. To 
assess their involvement in post-hemorrhagic complications, we determined the 
source and time-course of the release of inflammatory cytokines and acute-phase 
proteins in cerebrospinal fluid (CSF) following SAH. Concentrations of 
interleukin (IL)- 1beta, IL-6, transforming growth factor-beta1 (TGF-beta1) and 
C-reactive protein (CRP) in CSF of 36 patients with SAH were measured by 
enzyme-linked immunoabsorbent assay (ELISA). Floating cells collected from the 
CSF were centrifuged four to six days after SAH, and examined 
immunohistochemically. Intracellular IL-1beta and IL-6 were examined by flow 
cytometric analysis. The molecular weight of TGF-beta1 in CSF of 30 patients was 
examined by Western blot analysis. The TGF-beta1 levels of patients who had 
undergone ventriculoperitoneal (VP) shunt (n = 19) was significantly higher than 
nonshunt group (n = 16). The CRP levels of VP shunt group was significantly 
higher than nonshunt group. IL-6 concentration was maximal within day 0-1 and it 
was secreted by neutrophils and monocytes. ELISA showed consistently low levels 
of IL-1beta, whereas a proportion of monocytes and lymphcytes were IL- 
1beta-positive by flow cytometric analysis. TGF-beta1 levels were also maximal 
on day 0-1 according to ELISA, although it tended to be in the inactive form 
derived from platelets. A 25 kDa band of TGF-1 was detectable for at least 13 
days after SAH, which may have been secreted in part by neutrophils and 
monocytes. CRP levels in CSF peaked on day 2-3. The present results suggest that 
leukocytes induced by SAH play an important role in post-hemorrhagic 
inflammation in the subarachnoid space by releasing IL-6 and TGF-beta1. The CRP 
and TGF-beta1 levels in CSF are strongly concerned with communicating 
hydrocephalus after SAH.