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Potentiation of HIV-1 expression in microglial cells by nicotine: involvement of transforming growth factor-beta 1
R Bryan Rock1, Genya Gekker, Rajagopal N Aravalli
1Center for Infectious Diseases and Microbiology Translational Research, Division of Infectious Diseases and International Medicine, Department of Medicine, University of Minnesota Medical School, Minneapolis, MN 55455, USA. rockx012@umn.edu
Abstract:
HIV-1 infection and nicotine addiction are global public health crises. In the central nervous system, HIV-1 causes a devastating neurodegenerative disease. It is well recognized that microglial cells play a pivotal role in the neuropathogenesis of HIV-1 and that drugs of abuse not only contribute to the spread of this agent but may facilitate viral expression in these brain macrophages. Nicotine has been shown to stimulate the production of HIV-1 by in vitro-infected alveolar macrophages, and the HIV-1 protein gp120 binds to nicotinic receptors. In this study, we demonstrated the constitutive expression of nicotinic acetylcholine receptor mRNA in primary human microglial cells and showed that the pretreatment of microglia with nicotine increased HIV-1 expression in a concentration-dependent manner, as measured by p24 antigen levels in culture supernatants. We also found that nicotine robustly altered the gene expression profile of HIV-1-infected microglia and that the transforming growth factor-beta1 is involved in the enhanced expression of HIV-1 by nicotine.
Insights
Nicotine exposure increases HIV-1 expression in human microglial cells, potentially worsening neuroinflammation. This study highlights the role of nicotinic receptors and transforming growth factor-beta1 in this interaction, impacting HIV-1 neuropathogenesis.
Area of Science:
- Neuroscience
- Immunology
- Virology
Background:
- HIV-1 infection and nicotine addiction are significant global health issues.
- Microglial cells are crucial in HIV-1 neuropathogenesis, and substance abuse can exacerbate viral expression.
- Nicotine interacts with HIV-1, as evidenced by gp120 binding to nicotinic receptors.
Purpose of the Study:
- To investigate the effect of nicotine on HIV-1 expression in primary human microglial cells.
- To explore the role of nicotinic acetylcholine receptors in nicotine-induced HIV-1 enhancement.
- To identify molecular mechanisms, such as transforming growth factor-beta1, involved in this process.
Main Methods:
- Demonstrated constitutive expression of nicotinic acetylcholine receptor mRNA in human microglia.
- Quantified HIV-1 expression (p24 antigen levels) in nicotine-pretreated microglia.
- Analyzed gene expression profiles of HIV-1-infected microglia exposed to nicotine.
Main Results:
- Nicotine pretreatment increased HIV-1 expression in microglia in a dose-dependent manner.
- Nicotine significantly altered the gene expression profile of HIV-1-infected microglia.
- Transforming growth factor-beta1 was identified as a factor in nicotine-enhanced HIV-1 expression.
Conclusions:
- Nicotinic receptors in microglia are involved in regulating HIV-1 expression.
- Nicotine can enhance HIV-1 replication in the brain, potentially contributing to neuroinflammation.
- Targeting nicotinic pathways may offer new therapeutic strategies for HIV-1-associated neurodegeneration.
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