Cerebrospinal fluid soluble Fas and Fas ligand levels after aneurysmal subarachnoid haemorrhage

被引:0
作者
Kafadar, A. M. [1 ]
Uzan, M. [1 ]
Tanriverdi, T. [1 ]
Sanus, G. Z. [1 ]
Uzun, H. [2 ]
Kaynar, M. Y. [1 ]
Kuday, C. [1 ]
机构
[1] Istanbul Univ, Dept Neurosurg, PK 4 Cerrahpasa, TR-34301 Istanbul, Turkey
[2] Istanbul Univ, Dept Biochem, Istanbul, Turkey
来源
CEREBRAL VASOSPASM: NEW STRATEGIES IN RESEARCH AND TREATMENT | 2008年 / 104卷
关键词
aneurysms; apoptosis; cytokines; sFas; FasL; subarachnoid haemorrhage;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background. The aim of the present study was to show the CSF release of soluble Fas (sFas) and Fas Ligand (FasL) and their serum levels after subarachnoid haemorrhage (SAH) as potentially regulatory factors of programmed cell death (PCD). Method. Twelve SAH patients were studied prospectively on days 1 to 3, 5 and 7, with clinical evaluation and analysis of CSF and serum levels of sFas, FasL, IL-1, IL-6 and TNF-alpha. The control group consisted of eight patients with hydrocephalus. Findings. The CSF levels of sFas and FasL increased significantly, with a maximal increase at day 7 (p < 0.001) in SAH patients compared to control group. Serum sFas and FasL levels did not elevate significantly until day 7 (p < 0.05). In addition, CSF and serum levels of IL-1, IL-6 and TNF-a increased significantly. However, there was no correlation between CSF levels of sFas and FasL and IL-1, IL-6 and TNF-alpha. Conclusions. Our preliminary study demonstrates that sFas and FasL are present in higher amounts in CSF after aneurysmal SAH, suggesting that activation of the extrisic pathway of PCD may be initiated as a direct result of SAH independently from the posthaemorrhagic inflammatory response.
引用
收藏
页码:17 / +
页数:3
相关论文
共 20 条
[1]  
Bechmann I, 2000, GLIA, V32, P25, DOI 10.1002/1098-1136(200010)32:1<25::AID-GLIA30>3.0.CO
[2]  
2-Y
[3]   PROTECTION FROM FAS-MEDIATED APOPTOSIS BY A SOLUBLE FORM OF THE FAS MOLECULE [J].
CHENG, JH ;
ZHOU, T ;
LIU, CD ;
SHAPIRO, JP ;
BRAUER, MJ ;
KIEFER, MC ;
BARR, PJ ;
MOUNTZ, JD .
SCIENCE, 1994, 263 (5154) :1759-1762
[4]  
CHIO C, 2004, BRAIN RES REV, V44, P65
[5]  
Choi C, 1999, J IMMUNOL, V162, P1889
[6]   Correlates of p53- and Fas (CD95)-mediated apoptosis in Alzheimer's disease [J].
delaMonte, SM ;
Sohn, YK ;
Wands, JR .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 1997, 152 (01) :73-83
[7]   Multiple sclerosis: Fas signaling in oligodendrocyte cell death [J].
DSouza, SD ;
Bonetti, B ;
Balasingam, V ;
Cashman, NR ;
Barker, PA ;
Troutt, AB ;
Raine, CS ;
Antel, JP .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 184 (06) :2361-2370
[8]   Cerebral vasospasm after subarachnoid hemorrhage: Putative role of inflammation [J].
Dumont, AS ;
Dumont, RJ ;
Chow, MM ;
Lin, CL ;
Calisaneller, T ;
Ley, KF ;
Kassell, NF ;
Lee, KS .
NEUROSURGERY, 2003, 53 (01) :123-133
[9]   Detectable concentrations of Fas ligand in cerebrospinal fluid after severe head injury [J].
Ertel, W ;
Keel, M ;
Stocker, R ;
Imhof, HG ;
Leist, M ;
Steckholzer, U ;
Tanaka, M ;
Trentz, O ;
Nagata, S .
JOURNAL OF NEUROIMMUNOLOGY, 1997, 80 (1-2) :93-96
[10]   Increased cerebrospinal fluid concentrations of soluble Fas (CD95/Apo-1) in hydrocephalus [J].
Felderhoff-Mueser, U ;
Herold, R ;
Hochhaus, F ;
Koehne, P ;
Ring-Mrozik, E ;
Obladen, M ;
Bührer, C .
ARCHIVES OF DISEASE IN CHILDHOOD, 2001, 84 (04) :369-372