Potentiation of HIV-1 Expression in Microglial Cells by Nicotine: Involvement of Transforming Growth Factor-β1
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 t...
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| Veröffentlicht in: | Journal of neuroimmune pharmacology 2008-09, Vol.3 (3), p.143-149 |
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| container_title | Journal of neuroimmune pharmacology |
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| creator | Rock, R. Bryan Gekker, Genya Aravalli, Rajagopal N. Hu, Shuxian Sheng, Wen S. Peterson, Phillip K. |
| description | 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. |
| doi_str_mv | 10.1007/s11481-007-9098-7 |
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Bryan ; Gekker, Genya ; Aravalli, Rajagopal N. ; Hu, Shuxian ; Sheng, Wen S. ; Peterson, Phillip K.</creator><creatorcontrib>Rock, R. Bryan ; Gekker, Genya ; Aravalli, Rajagopal N. ; Hu, Shuxian ; Sheng, Wen S. ; Peterson, Phillip K.</creatorcontrib><description>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. 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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.</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brief Report</subject><subject>Cell Biology</subject><subject>Gene expression</subject><subject>Growth factors</subject><subject>Immunology</subject><subject>Neurosciences</subject><subject>Nicotine</subject><subject>Pharmacology/Toxicology</subject><subject>Virology</subject><issn>1557-1890</issn><issn>1557-1904</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp1kc1O3DAUhS3UCijtA3RnqevQe5M4sbuoVI34GQnaLmi3lsc_g1HGntqZAV6LB-GZcDQU0UVXPrLv-e6RDyEfEY4RoP-cEVuOVZGVAMGrfo8cImN9hQLaN381F3BA3uV8A9C2LcA-OUAOHTBeH5L4M442jF6NPgYaHT2f_66Qntytk815uvOBXnqd4nLwaqAzOwyZLu7pd6_j6IP9QudhG4etXRXMBLhKKmQX08qHJT1L8Xa8pqdKjzFVjw_4nrx1asj2w_N5RH6dnlzNzquLH2fz2beLSjeihDYOOtM5bRrsG-EQDBPaau0MW7iGc25M1zMnjOW10qxWYDoUziIDzRRbNEfk64673ixW1ugSLqlBrpNfqXQvo_Ly35fgr-UybiVv-la0ogA-PQNS_LOxeZQ3cZNCySxRMOB117VQpnA3VT4o52TdywYEOXUkdx3JSU4dyb546p0nl9mwtOkV-b-mJ0Sjlbc</recordid><startdate>200809</startdate><enddate>200809</enddate><creator>Rock, R. 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Bryan</creatorcontrib><creatorcontrib>Gekker, Genya</creatorcontrib><creatorcontrib>Aravalli, Rajagopal N.</creatorcontrib><creatorcontrib>Hu, Shuxian</creatorcontrib><creatorcontrib>Sheng, Wen S.</creatorcontrib><creatorcontrib>Peterson, Phillip K.</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neuroimmune pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rock, R. 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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. 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| subjects | Biomedical and Life Sciences Biomedicine Brief Report Cell Biology Gene expression Growth factors Immunology Neurosciences Nicotine Pharmacology/Toxicology Virology |
| title | Potentiation of HIV-1 Expression in Microglial Cells by Nicotine: Involvement of Transforming Growth Factor-β1 |
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