Potentiation of HIV-1 expression in microglial cells by nicotine: Involvement of transforming growth factor-β1

R B Rock; Genya Gekker; Raj Aravalli; Shuxian Hu; Wen Sheng; Phillip K. Peterson

doi:10.1007/s11481-007-9098-7

Potentiation of HIV-1 expression in microglial cells by nicotine: Involvement of transforming growth factor-β1

R B Rock, Genya Gekker, Raj Aravalli, Shuxian Hu, Wen Sheng, Phillip K. Peterson

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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-β1 is involved in the enhanced expression of HIV-1 by nicotine.

Original language	English (US)
Pages (from-to)	143-149
Number of pages	7
Journal	Journal of Neuroimmune Pharmacology
Volume	3
Issue number	3
DOIs	https://doi.org/10.1007/s11481-007-9098-7
State	Published - Sep 2008

Bibliographical note

Funding Information:
Acknowledgments This work was supported by grants from National Institute on Drug Abuse, DA-020398, and was also supported in part by the U.S. Public Health Service grant DA020398.

Keywords

HIV-1
Microglia
Neuropathogenesis
Nicotine
TGF-β1

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title = "Potentiation of HIV-1 expression in microglial cells by nicotine: Involvement of transforming growth factor-β1",

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-β1 is involved in the enhanced expression of HIV-1 by nicotine.",

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note = "Funding Information: Acknowledgments This work was supported by grants from National Institute on Drug Abuse, DA-020398, and was also supported in part by the U.S. Public Health Service grant DA020398.",

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AU - Sheng, Wen

AU - Peterson, Phillip K.

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N2 - 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-β1 is involved in the enhanced expression of HIV-1 by nicotine.

AB - 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-β1 is involved in the enhanced expression of HIV-1 by nicotine.

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Potentiation of HIV-1 expression in microglial cells by nicotine: Involvement of transforming growth factor-β1

Abstract

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