In vivo neutralization of endogenous brain fractalkine increases hippocampal TNFα and 8-isoprostane production induced by intracerebroventricular injection of LPS

被引：83

作者：

Zujovic, V ^{[1
]}

Schussler, N ^{[1
]}

Jourdain, D ^{[1
]}

Duverger, D ^{[1
]}

Taupin, V ^{[1
]}

机构：

[1] Sanofi Synthelabo, CNS Res Dept, F-92225 Bagneux, France

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2001年 / 115卷 / 1-2期

关键词：

fractalkine; LPS; intracerebroventricular injection; TNF-alpha; 8-isoprostanes;

D O I：

10.1016/S0165-5728(01)00259-4

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Fractalkine is a chemokine widely and constitutively expressed in the brain and, as suggested by in vitro studies, it is involved in brain inflammatory responses. In this study, we have investigated the in vivo anti-inflammatory potential of fractalkine in a model of neuroinflammation induced by intracerebroventricular injection of lipopolysaccharide (LPS) in rats. LPS induces a rapid and acute production of the pro-inflammatory cytokine, TNF alpha, in hippocampus and cerebrospinal fluid (CSF), and an increase of 8-isoprostane levels, a marker of oxidative stress, in hippocampus. Although intracerebroventricular injection of fractalkine has no effect on TNF alpha and 8-isoprostane production, neutralization of endogenous fractalkine within the brain with a specific anti-fractalkine antibody potentiates LPS effects. These data emphasize the involvement of constitutive brain fractalkine in the control of inflammatory reaction in CNS. (C) 2001 Elsevier Science B.V. All rights reserved.

引用

页码：135 / 143

页数：9

共 42 条

[1] THE ACUTE INFLAMMATORY RESPONSE TO LIPOPOLYSACCHARIDE IN CNS PARENCHYMA DIFFERS FROM THAT IN OTHER BODY-TISSUES [J].

ANDERSSON, PB ;

PERRY, VH ;

GORDON, S .

NEUROSCIENCE, 1992, 48 (01) :169-186

[2] Chemokines in the CNS: plurifunctional mediators in diverse states [J].

Asensio, VC ;

Campbell, IL .

TRENDS IN NEUROSCIENCES, 1999, 22 (11) :504-512

[3] CYTOTOXICITY OF MICROGLIA [J].

BANATI, RB ;

GEHRMANN, J ;

SCHUBERT, P ;

KREUTZBERG, GW .

GLIA, 1993, 7 (01) :111-118

[4] TUMOR NECROSIS, CACHEXIA, SHOCK, AND INFLAMMATION - A COMMON MEDIATOR [J].

BEUTLER, B ;

CERAMI, A .

ANNUAL REVIEW OF BIOCHEMISTRY, 1988, 57 :505-518

[5] The chemokine fractalkine inhibits Fas-mediated cell death of brain microglia [J].

Boehme, SA ;

Lio, FM ;

Maciejewski-Lenoir, D ;

Bacon, KB ;

Conlon, PJ .

JOURNAL OF IMMUNOLOGY, 2000, 165 (01) :397-403

[6] Glia-dependent neurotoxicity and neuroprotection in mesencephalic cultures [J].

Bronstein, DM ;

PerezOtano, I ;

Sun, V ;

Sawin, SBM ;

Chan, J ;

Wu, GC ;

Hudson, PM ;

Kong, LY ;

Hong, JS ;

McMillian, MK .

BRAIN RESEARCH, 1995, 704 (01) :112-116

[7] Fractalkine cleavage from neuronal membranes represents an acute event in the inflammatory response to excitotoxic brain damage [J].

Chapman, GA ;

Moores, K ;

Harrison, D ;

Campbell, CA ;

Stewart, BR ;

Strijbos, PJLM .

JOURNAL OF NEUROSCIENCE, 2000, 20 (15)

[8] INDEPENDENT DOWN-REGULATION OF CENTRAL AND PERIPHERAL TUMOR-NECROSIS-FACTOR PRODUCTION AS A RESULT OF LIPOPOLYSACCHARIDE TOLERANCE IN MICE [J].

FAGGIONI, R ;

FANTUZZI, G ;

VILLA, P ;

BUURMAN, W ;

VANTITS, LJH ;

GHEZZI, P .

INFECTION AND IMMUNITY, 1995, 63 (04) :1473-1477

[9] FORMATION OF F-2-ISOPROSTANES DURING AORTIC ENDOTHELIAL CELL-MEDIATED OXIDATION OF LOW-DENSITY-LIPOPROTEIN [J].

GOPAUL, NK ;

NOUROOZZADEH, J ;

MALLET, AI ;

ANGGARD, EE .

FEBS LETTERS, 1994, 348 (03) :297-300

[10] Role for neuronally derived fractalkine in mediating interactions between neurons and CX3CR1-expressing microglia [J].

Harrison, JK ;

Jiang, Y ;

Chen, SZ ;

Xia, YY ;

Maciejewski, D ;

McNamara, RK ;

Streit, WJ ;

Salafranca, MN ;

Adhikari, S ;

Thompson, DA ;

Botti, P ;

Bacon, KB ;

Feng, LL .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (18) :10896-10901

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