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Title:
Impact of Opiate–HIV-1 Interactions on Neurotoxic Signaling | Journal of Neuroimmune Pharmacology
Description:
Opiate drug abuse exacerbates the pathogenesis of human immunodeficiency virus-1 (HIV-1) in the central nervous system through direct actions on glia and neurons. Opiate abuse causes widespread disruption of astroglial and microglial function, and significant increases in astroglial-derived proinflammatory cytokines and chemokines, which likely contributes to neuronal dysfunction, death, and HIV encephalitis. Neurons are also directly affected by opiate–HIV-1 interactions. HIV-1 and the viral proteins gp120 and Tat activate multiple caspase-dependent and caspase-independent proapoptotic pathways in neurons involving phosphatidylinositol 3-kinase (PI3 kinase)/Akt, as well as p38, c-Jun N-terminal kinase (JNK) and/or other mitogen-activated protein kinases (MAPKs). Opiates appear to decrease the threshold for HIV-1-mediated neurotoxicity by sending convergent signals that exacerbate proapoptotic events induced by viral and cellular toxic products. The synergistic proinflammatory and neurotoxic effects of opiate drugs on glia and neurons are largely mediated through μ opioid receptors, which are expressed by subpopulations of astroglia, microglia, and neurons. Opiate abuse intrinsically modifies the host response to HIV-1. Identification of how this occurs is providing considerable insight toward understanding the mechanisms underlying HIV-1-associated dementia.
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Keywords {🔍}
google, scholar, pubmed, cas, article, hiv, kinase, protein, cell, nath, neurons, apoptosis, hauser, human, tat, biol, activation, dementia, survival, knapp, aids, death, science, signaling, elhage, immunodeficiency, virus, neurotoxicity, regulation, neurosci, abuse, microglial, neuronal, pathways, phosphatidylinositol, morphine, exp, chem, opiate, drug, jnk, mitogenactivated, access, astrocytes, caspase, res, akt, involvement, pathway, privacy,
Topics {✒️}
c-jun n-terminal kinase altering g-protein–effector interactions ifn-gamma-inducible protein-10 expression μ opioid receptors pkb/akt-dependent cell survival month download article/chapter morphine-induced macrophage apoptosis serine/threonine protein kinases monocyte chemoattractant protein-1 mitogen-activated protein kinase mitogen-activated protein kinases protein-coupled opiate receptor fas–fas ligand interaction human microglial cells stress-activated map kinase seizure-induced neuronal death phosphatidylinositol 3-kinase/akt-dependent phosphatidylinositol 3-kinase-akt pathway protein-coupled receptors receptor-regulated mapk scaffold nerve growth factor apoptosis signal-regulating kinase pre-symptomatic hiv infection cell-intrinsic death machinery hiv-1 tat-mediated activation caspase-independent proapoptotic pathways mitogen-activated protein mu-opioid induction full article pdf hiv-1 tat-stimulated astrocytes astroglial-derived proinflammatory cytokines tat-mediated neurotoxicity gp120-induced apoptosis hiv-1-mediated neurotoxicity ca2+-dependent mechanism related subjects induced superoxide production akt protein kinase akt/protein kinase kappa-opioid modulation opioid system diversity morphine enhances interleukin-12 pi3-kinase gamma cxcr4-mediated chemotaxis human immunodeficiency virus-1 human immunodeficiency virus human immunodeficiency virus enhanced morphine analgesia morphine stimulates phagocytosis privacy choices/manage cookies
Questions {❓}
- Anthony IC, Ramage SN, Carnie FW, Simmonds P, Bell JE (2005) Does drug abuse alter microglial phenotype and cell turnover in the context of advancing HIV infection?
- Arango JC, Simmonds P, Brettle RP, Bell JE (2004) Does drug abuse influence the microglial response in AIDS and HIV encephalitis?
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headline:Impact of Opiate–HIV-1 Interactions on Neurotoxic Signaling
description:Opiate drug abuse exacerbates the pathogenesis of human immunodeficiency virus-1 (HIV-1) in the central nervous system through direct actions on glia and neurons. Opiate abuse causes widespread disruption of astroglial and microglial function, and significant increases in astroglial-derived proinflammatory cytokines and chemokines, which likely contributes to neuronal dysfunction, death, and HIV encephalitis. Neurons are also directly affected by opiate–HIV-1 interactions. HIV-1 and the viral proteins gp120 and Tat activate multiple caspase-dependent and caspase-independent proapoptotic pathways in neurons involving phosphatidylinositol 3-kinase (PI3 kinase)/Akt, as well as p38, c-Jun N-terminal kinase (JNK) and/or other mitogen-activated protein kinases (MAPKs). Opiates appear to decrease the threshold for HIV-1-mediated neurotoxicity by sending convergent signals that exacerbate proapoptotic events induced by viral and cellular toxic products. The synergistic proinflammatory and neurotoxic effects of opiate drugs on glia and neurons are largely mediated through μ opioid receptors, which are expressed by subpopulations of astroglia, microglia, and neurons. Opiate abuse intrinsically modifies the host response to HIV-1. Identification of how this occurs is providing considerable insight toward understanding the mechanisms underlying HIV-1-associated dementia.
datePublished:2006-02-24T00:00:00Z
dateModified:2006-02-24T00:00:00Z
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headline:Impact of Opiate–HIV-1 Interactions on Neurotoxic Signaling
description:Opiate drug abuse exacerbates the pathogenesis of human immunodeficiency virus-1 (HIV-1) in the central nervous system through direct actions on glia and neurons. Opiate abuse causes widespread disruption of astroglial and microglial function, and significant increases in astroglial-derived proinflammatory cytokines and chemokines, which likely contributes to neuronal dysfunction, death, and HIV encephalitis. Neurons are also directly affected by opiate–HIV-1 interactions. HIV-1 and the viral proteins gp120 and Tat activate multiple caspase-dependent and caspase-independent proapoptotic pathways in neurons involving phosphatidylinositol 3-kinase (PI3 kinase)/Akt, as well as p38, c-Jun N-terminal kinase (JNK) and/or other mitogen-activated protein kinases (MAPKs). Opiates appear to decrease the threshold for HIV-1-mediated neurotoxicity by sending convergent signals that exacerbate proapoptotic events induced by viral and cellular toxic products. The synergistic proinflammatory and neurotoxic effects of opiate drugs on glia and neurons are largely mediated through μ opioid receptors, which are expressed by subpopulations of astroglia, microglia, and neurons. Opiate abuse intrinsically modifies the host response to HIV-1. Identification of how this occurs is providing considerable insight toward understanding the mechanisms underlying HIV-1-associated dementia.
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μ-opioid receptors
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neuroimmunology
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