Increased cytokine release from peripheral blood cells after acute stroke

被引:189
作者
Ferrarese, C
Mascarucci, P
Zoia, C
Cavarretta, G
Frigo, M
Begni, B
Sarinella, F
Frattola, L
De Simoni, MG
机构
[1] Univ Milan, Dept Neurol, Osped San Gerardo, I-20052 Monza, Italy
[2] Univ Milan, Dept Anat, Osped San Gerardo, I-20052 Monza, Italy
[3] Sci Inst E Medea, Milan, Italy
[4] Sci Inst Bosisio Parini, Milan, Italy
[5] Sci Inst Lecco, Milan, Italy
[6] Sci Inst Don C Gnocchi, Milan, Italy
[7] Mario Negri Inst Pharmacol Res, Dept Neurosci, Milan, Italy
关键词
cytokine; brain ischemia; blood cells; serum;
D O I
10.1097/00004647-199909000-00008
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha can play pathogenetic or protective roles in stroke. They are increased in the brain after experimental ischemia and in the CSF of patients with stroke. However, their presence in the periphery is still controversial. To determine the source and lime-course of cytokines in blood of stroke patients, IL-6 and TNF-alpha release from blood cells and serum levels were determined in 40 patients on days 1 through 2, 4, 10, 30, and 90 after stroke. Twenty healthy age-matched volunteers were used as controls. IL-6 and TNF-alpha release from stimulated blood cells was increased in stroke patients, compared to controls. A peak response (+224%) was observed at day 4 for IL-6, while TNF-alpha release was largely and significantly increased (about three-fold compared to controls) from day 1 to 2 until day 90 after stroke. The increase in IL-6 release was significantly higher in ischemic, compared to hemorragic strokes, at days 1 and 1. Circulating IL-6 was increased at each time point. The ischemic processes in the CNS induces a long-lasting activation of IL-6 and TNF-alpha production in peripheral blood cells, which are a major source of serum cytokines after stroke.
引用
收藏
页码:1004 / 1009
页数:6
相关论文
共 40 条
[1]   PENETRATION OF INTERLEUKIN-6 ACROSS THE MURINE BLOOD-BRAIN-BARRIER [J].
BANKS, WA ;
KASTIN, AJ ;
GUTIERREZ, EG .
NEUROSCIENCE LETTERS, 1994, 179 (1-2) :53-56
[2]   Persistent inflammatory response in stroke survivors [J].
Beamer, NB ;
Coull, BM ;
Clark, WM ;
Briley, DP ;
Wynn, M ;
Sexton, G .
NEUROLOGY, 1998, 50 (06) :1722-1728
[3]   INTERLEUKIN-6 AND INTERLEUKIN-1 RECEPTOR ANTAGONIST IN ACUTE STROKE [J].
BEAMER, NB ;
COULL, BM ;
CLARK, WM ;
HAZEL, JS ;
SILBERGER, JR .
ANNALS OF NEUROLOGY, 1995, 37 (06) :800-805
[4]   MEASUREMENTS OF ACUTE CEREBRAL INFARCTION - A CLINICAL EXAMINATION SCALE [J].
BROTT, T ;
ADAMS, HP ;
OLINGER, CP ;
MARLER, JR ;
BARSAN, WG ;
BILLER, J ;
SPILKER, J ;
HOLLERAN, R ;
EBERLE, R ;
HERTZBERG, V ;
RORICK, M ;
MOOMAW, CJ ;
WALKER, M .
STROKE, 1989, 20 (07) :864-870
[5]   Altered neuronal and microglial responses to excitotoxic and ischemic brain injury in mice lacking TNF receptors [J].
Bruce, AJ ;
Boling, W ;
Kindy, MS ;
Peschon, J ;
Kraemer, PJ ;
Carpenter, MK ;
Holtsberg, FW ;
Mattson, MP .
NATURE MEDICINE, 1996, 2 (07) :788-794
[6]   INDUCTION OF INTERLEUKIN-1-BETA MESSENGER-RNA AFTER FOCAL CEREBRAL-ISCHEMIA IN THE RAT [J].
BUTTINI, M ;
SAUTER, A ;
BODDEKE, HWGM .
MOLECULAR BRAIN RESEARCH, 1994, 23 (1-2) :126-134
[7]   Ischemic tolerance in the brain [J].
Chen, J ;
Simon, R .
NEUROLOGY, 1997, 48 (02) :306-311
[8]   Cytokines and reperfusion injury [J].
Clark, WM .
NEUROLOGY, 1997, 49 (05) :S10-S14
[9]  
De Simoni MG, 1997, NEUROSCI RES COMMUN, V21, P163
[10]  
DEGRABA T, 1996, CEREBROVASC DIS, V6, P10