Neuroinflammatory responses from microglia recovered from HIV-1-infected and seronegative subjects

被引:24
作者
Ghorpade, A
Persidsky, Y
Swindells, S
Borgmann, K
Persidsky, R
Holter, S
Cotter, R
Gendelman, HE
机构
[1] Univ Nebraska, Lab Cellular Neuroimmunol, Med Ctr, Omaha, NE 68198 USA
[2] Univ Nebraska, Neuropathol Lab, Med Ctr, Omaha, NE 68198 USA
[3] Univ Nebraska, Lab Neuroregenerat, Med Ctr, Omaha, NE 68198 USA
[4] Univ Nebraska, Ctr Neurovirol & Neurodegenerat Disorders, Med Ctr, Omaha, NE 68198 USA
[5] Univ Nebraska, Dept Pharmacol, Med Ctr, Omaha, NE 68198 USA
[6] Univ Nebraska, Dept Pathol & Microbiol, Med Ctr, Omaha, NE 68198 USA
[7] Univ Nebraska, Dept Biochem & Mol Biol, Med Ctr, Omaha, NE 68198 USA
[8] Univ Nebraska, Dept Internal Med, Med Ctr, Omaha, NE 68198 USA
关键词
HIV-1-associated dementia; microglia activation; rapid autopsy; chronic inflammation;
D O I
10.1016/j.jneuroim.2005.01.022
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Microglial and macrophage infection and immune activation underlie the pathogenesis of HIV-1-associated dementia (HAD). To assess microglial function in HAD, we isolated cells from brain tissues recovered from an HIV-1-infected patient within 4 h of death. Brain tissue from seronegative patients served as controls. Regional neuropathology was correlated to microglial function. HlV-1-patient microglia formed multinucleated giant cells and produced progeny virions. These microglia secreted reduced basal and LPS-stimulated TNF-alpha levels compared to controls. Monocytes from seronegative donors paralleled these diminished immune responses following repeated LPS-activation. These results demonstrate changes in innate microglial function following viral infection or chronic immune activation. (C) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:145 / 156
页数:12
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