Neuronal injury regulates fractalkine: relevance for HIV-1 associated dementia

被引:65
作者
Erichsen, D
Lopez, AL
Peng, H
Niemann, D
Williams, C
Bauer, M
Morgello, S
Cotter, RL
Ryan, LA
Ghorpade, A
Gendelman, HE
Zheng, JL
机构
[1] Univ Nebraska, Med Ctr, Ctr Neurovirol & Neurodegenerat Disorders, Lab Neurotoxicol, Omaha, NE 68198 USA
[2] Univ Nebraska, Med Ctr, Dept Pathol & Microbiol, Omaha, NE 68198 USA
[3] Mt Sinai Med Ctr, New York, NY 10029 USA
[4] Univ Nebraska, Med Ctr, Dept Med, Omaha, NE 68198 USA
[5] Univ Nebraska, Med Ctr, Dept Pharmacol, Omaha, NE 68198 USA
关键词
chemokines; fractalkine; macrophage; HIV-1 associated dementia; inflammation;
D O I
10.1016/S0165-5728(03)00117-6
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 (FKN), a chemokine highly expressed in the central nervous system, participates in inflammatory responses operative in many brain disorders including HIV-1 associated dementia (HAD). In this report, HIV-1 progeny virions and pro-inflammatory products led to FKN production associated with neuronal injury and apoptosis. FKN was produced by neurons and astrocytes; but differentially produced by the two cell types. Laboratory tests paralleled those in infected people where cerebrospinal fluid FKN levels in HIV-1 infected cognitively impaired (n = 16) patients were found to be increased when compared to infected patients without cognitive impairment (n = 8, P = 0.0345). These results demonstrate a possible role of FKN in HAD pathogenesis. (C) 2003 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:144 / 155
页数:12
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