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Neuroinflammatory responses from microglia recovered from HIV-1-infected and seronegative subjects
Anuja Ghorpade1, Yury Persidsky, Susan Swindells
1Laboratory of Cellular Neuroimmunology, 985215 Nebraska Medical Center, Omaha, NE, 68198-5215, USA. aghorpad@unmc.edu
Abstract:
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-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.
Insights
HIV-1-associated dementia (HAD) involves brain immune cell dysfunction. Researchers found that microglia from HIV-1 patients showed altered immune responses, impacting innate immunity in the brain.
Area of Science:
- Neuroscience
- Immunology
- Virology
Background:
- HIV-1-associated dementia (HAD) pathogenesis involves microglial and macrophage infection and immune activation.
- Understanding microglial function is crucial for HAD research.
Purpose of the Study:
- To assess microglial function in the context of HIV-1-associated dementia.
- To investigate changes in innate immune responses of microglia during HIV-1 infection.
Main Methods:
- Isolation of microglial cells from post-mortem brain tissues of an HIV-1 infected patient and seronegative controls.
- Correlation of regional neuropathology with microglial function.
- Assessment of TNF-alpha secretion (basal and LPS-stimulated) in microglia.
- Evaluation of monocyte immune responses following repeated LPS activation.
Main Results:
- Microglia from the HIV-1 patient formed multinucleated giant cells and produced HIV-1 virions.
- These HIV-1 patient microglia exhibited reduced basal and LPS-stimulated TNF-alpha secretion compared to controls.
- Monocytes from seronegative donors showed similar diminished immune responses after repeated LPS stimulation.
Conclusions:
- Viral infection and chronic immune activation significantly alter innate microglial function.
- These findings highlight changes in microglial immune responses relevant to HIV-1-associated dementia pathogenesis.
