Differential regulation by cytokines of human astrocyte nitric oxide production

被引:78
作者
Hu, SX
Sheng, WS
Peterson, PK
Chao, CC
机构
[1] MINNEAPOLIS MED RES FDN INC,NEUROIMMUNOBIOL & HOST DEF LAB,MINNEAPOLIS,MN 55404
[2] UNIV MINNESOTA,SCH MED,MINNEAPOLIS,MN 55404
关键词
reactive nitrogen intermediates; interleukin-1; interferon-gamma; transforming growth factor-beta; interleukin-1 receptor antagonist protein;
D O I
10.1002/glia.440150412
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Reactive nitrogen intermediates, such as nitric oxide (NO), play an important role in host-defense and injury. Human astrocytes released abundant NO upon stimulation with the pro-inflammatory cytokine interleukin (IL)-1 beta, which was potentiated by interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha. IL-1 receptor antagonist protein markedly attenuated astrocyte NO production. The anti inflammatory cytokines IL-4 and IL-10 potently suppressed IL-1 beta plus IFN-gamma-stimulated NO, while transforming growth factor-beta preferentially inhibited IL-1 beta plus TNF-alpha-stimulated production of NO. These findings suggest that while IL-1 plays a key role in inducing astrocyte NO production, anti-inflammatory cytokines have the capacity to downregulate NO production by IL-l-stimulated astrocytes. (C) 1995 Wiley-Liss, Inc.
引用
收藏
页码:491 / 494
页数:4
相关论文
共 24 条
[1]   INFLAMMATORY CYTOKINES WITHIN THE CENTRAL-NERVOUS-SYSTEM - SOURCES, FUNCTION, AND MECHANISM OF ACTION [J].
BENVENISTE, EN .
AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 263 (01) :C1-C16
[2]   INDUCTION OF NITRIC-OXIDE SYNTHASE IN DEMYELINATING REGIONS OF MULTIPLE-SCLEROSIS BRAINS [J].
BO, L ;
DAWSON, TM ;
WESSELINGH, S ;
MORK, S ;
CHOI, S ;
KONG, PA ;
HANLEY, D ;
TRAPP, BD .
ANNALS OF NEUROLOGY, 1994, 36 (05) :778-786
[3]   MECHANISM OF SUPPRESSION OF NITRIC-OXIDE SYNTHASE EXPRESSION BY INTERLEUKIN-4 IN PRIMARY MOUSE MACROPHAGES [J].
BOGDAN, C ;
VODOVOTZ, Y ;
PAIK, J ;
XIE, QW ;
NATHAN, C .
JOURNAL OF LEUKOCYTE BIOLOGY, 1994, 55 (02) :227-233
[4]   TRANSFORMING GROWTH-FACTOR-BETA PROTECTS HUMAN NEURONS AGAINST BETA-AMYLOID-INDUCED INJURY [J].
CHAO, CC ;
HU, SX ;
KRAVITZ, FH ;
TSANG, M ;
ANDERSON, WR ;
PETERSON, PK .
MOLECULAR AND CHEMICAL NEUROPATHOLOGY, 1994, 23 (2-3) :159-178
[5]  
CHAO CC, 1993, J IMMUNOL, V151, P1473
[6]   EFFECTS OF TRANSFORMING GROWTH-FACTOR-BETA ON MURINE ASTROCYTE GLUTAMINE-SYNTHETASE ACTIVITY - IMPLICATIONS IN NEURONAL INJURY [J].
CHAO, CC ;
HU, SX ;
TSANG, M ;
WEATHERBEE, J ;
MOLITOR, TW ;
ANDERSON, WR ;
PETERSON, PK .
JOURNAL OF CLINICAL INVESTIGATION, 1992, 90 (05) :1786-1793
[7]  
CONSTAM DB, 1992, J IMMUNOL, V148, P1404
[8]   CERVICAL LYMPHATICS, THE BLOOD-BRAIN-BARRIER AND THE IMMUNOREACTIVITY OF THE BRAIN - A NEW VIEW [J].
CSERR, HF ;
KNOPF, PM .
IMMUNOLOGY TODAY, 1992, 13 (12) :507-512
[9]   GLIAL CELL-SPECIFIC MECHANISMS OF TGF-BETA-1 INDUCTION BY IL-1 IN CEREBRAL-CORTEX [J].
DACUNHA, A ;
JEFFERSON, JA ;
JACKSON, RW ;
VITKOVIC, L .
JOURNAL OF NEUROIMMUNOLOGY, 1993, 42 (01) :71-86
[10]   A NOVEL NEURONAL MESSENGER MOLECULE IN BRAIN - THE FREE-RADICAL, NITRIC-OXIDE [J].
DAWSON, TM ;
DAWSON, VL ;
SNYDER, SH .
ANNALS OF NEUROLOGY, 1992, 32 (03) :297-311