TY - JOUR
T1 - Neuroinflammatory responses from microglia recovered from HIV-1-infected and seronegative subjects
AU - Ghorpade, Anuja
AU - Persidsky, Yury
AU - Swindells, Susan
AU - Borgmann, Kathleen
AU - Persidsky, Raisa
AU - Holter, Spring
AU - Cotter, Robin
AU - Gendelman, Howard E.
N1 - Funding Information:
All the authors of these manuscripts thank the donor families for their contribution to this research effort and all members involved in running the Rapid Autopsy Program. We appreciate excellent administrative support from Ms. Robin Taylor and Ms. Julie Ditter. The authors thank Ms. Radhika Suryadevara for critical editing of the manuscript. This effort was supported, in part, through funding from 1 P01 NS43985-01A1 (PI, HEG; Core leader, AG), R01 NS 43113 to AG, R37 NS 36126 to HEG, Clinical Research Center and the University of Nebraska.
PY - 2005/6
Y1 - 2005/6
N2 - 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. HIV-1-patient microglia formed multinucleated giant cells and produced progeny virions. These microglia secreted reduced basal and LPS-stimulated TNF-α 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.
AB - 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. HIV-1-patient microglia formed multinucleated giant cells and produced progeny virions. These microglia secreted reduced basal and LPS-stimulated TNF-α 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.
KW - Chronic inflammation
KW - HIV-1-associated dementia
KW - Microglia activation
KW - Rapid autopsy
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U2 - 10.1016/j.jneuroim.2005.01.022
DO - 10.1016/j.jneuroim.2005.01.022
M3 - Article
C2 - 15869805
AN - SCOPUS:18944373187
SN - 0165-5728
VL - 163
SP - 145
EP - 156
JO - Advances in Neuroimmunology
JF - Advances in Neuroimmunology
IS - 1-2
ER -