Research Topics
Species | YURI VSEVOLODOVIC PERSIDSKYSummaryAffiliation: University of Nebraska Medical Center Country: USA Publications
Research Grants
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Detail Information
Publications
Microglial and astrocyte chemokines regulate monocyte migration through the blood-brain barrier in human immunodeficiency virus-1 encephalitisY Persidsky
Center for Neurovirology, Departments of Pathology, Eppley Institute for Cancer and Allied Diseases, University of Nebraska, Omaha, USA
Am J Pathol 155:1599-611. 1999..We conclude that microglial activation alone and/or through its interactions with astrocytes induces beta-chemokine-mediated monocyte migration in HAD...- Rodent model systems for studies of HIV-1 associated dementiaY Persidsky
Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, NE 68198, USA
Neurotox Res 8:91-106. 2005..The potential importance and limitations of the models in reflecting human disease are discussed with emphasis on their utility for development of therapies to combat HIV-1-associated neurologic impairment... - Rho-mediated regulation of tight junctions during monocyte migration across the blood-brain barrier in HIV-1 encephalitis (HIVE)Yuri Persidsky
Center for Neurovirology and Neurodegenerative Disorders, Nebraska Medical Center, Omaha, NE 68198 5215, USA
Blood 107:4770-80. 2006..Thus, loss of TJ integrity was associated with Rho activation caused by monocyte brain migration, suggesting that Rho/RhoK activation in BMVECs could be an underlying cause of BBB impairment during HIVE... - Mononuclear phagocyte immunity and the neuropathogenesis of HIV-1 infectionYuri Persidsky
Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198 5215, USA
J Leukoc Biol 74:691-701. 2003..New therapeutic strategies are discussed based on current knowledge of HIV-1-associated dementia pathogenesis... - Immune privilege and HIV-1 persistence in the CNSYuri Persidsky
Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, NE 68198 5215, USA
Immunol Rev 213:180-94. 2006..Understanding the immune-privileged state created by virus, the brain microenvironment, and the ability to enhance anti-viral immunity offer new therapeutic strategies for treatment of HIV-1 CNS infection... - Battle of animal modelsYuri Persidsky
Department of Pharmacology Experimental Neuroscience, University of Nebraska Medical Center, 985215 Nebraska Medical Center, Omaha, NE 68198 5215, USA
J Neuroimmune Pharmacol 2:171-7. 2007..It highlighted animal model relevance to human disease/condition, its utility for the studies of pathogenesis, potential importance for the development of therapeutics, and demonstrated limitations/pitfalls... - Murine models for human immunodeficiency virus type 1-associated dementia: the development of new treatment testing paradigmsYuri Persidsky
Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, Nebraska 68198 5215, USA
J Neurovirol 8:49-52. 2002.... - Blood-brain barrier: structural components and function under physiologic and pathologic conditionsYuri Persidsky
Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, NE 68198 5215, USA
J Neuroimmune Pharmacol 1:223-36. 2006..Better understanding of tight junction regulation and factors affecting transport systems will allow the development of therapeutics to improve the BBB function in health and disease... - Reduction in glial immunity and neuropathology by a PAF antagonist and an MMP and TNFalpha inhibitor in SCID mice with HIV-1 encephalitisY Persidsky
The Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, 985215 Nebraska Medical Center, Omaha, NE 68198 5215, USA
J Neuroimmunol 114:57-68. 2001..These findings demonstrate that reduction of brain inflammatory responses, independent of viral replication, can affect HIVE pathology in an animal model system of disease... - Mononuclear phagocytes mediate blood-brain barrier compromise and neuronal injury during HIV-1-associated dementiaY Persidsky
Center for Neurovirology and Neurodegenerative Disorders, The Department of Pathology, University of Nebraska Medical Center, Omaha 68198 5215, USA
J Leukoc Biol 68:413-22. 2000..In toto, these works underscore the diverse roles of chemokines in HIV-1 neuropathogenesis and lay the foundation for future therapeutic interventions... - Ethanol-induced activation of myosin light chain kinase leads to dysfunction of tight junctions and blood-brain barrier compromiseJames Haorah
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology, University of Nebraska Medical Center, Omaha, NE 68198, USA
Alcohol Clin Exp Res 29:999-1009. 2005..Cytoskeletal alterations (MLC) and TJ changes (occludin and claudin-5 phosphorylation) result in BBB impairment (decrease in TEER). TJ compromise is associated with increased monocyte migration across the BBB... - Alcohol abuse enhances neuroinflammation and impairs immune responses in an animal model of human immunodeficiency virus-1 encephalitisRaghava Potula
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology and Experimental Neuroscience, 985215 Nebraska Medical Center, Omaha, NE 68198-5215, USA
Am J Pathol 168:1335-44. 2006..Thus, alcohol abuse could be a co-factor in progression of HIV-1 infection of the brain... - HIV-1 infected monocyte-derived macrophages affect the human brain microvascular endothelial cell proteome: new insights into blood-brain barrier dysfunction for HIV-1-associated dementiaMary Ricardo-Dukelow
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198 5215, USA
J Neuroimmunol 185:37-46. 2007..Results were validated by Western blot analysis. We conclude that HIV-1-infected MDM affect the HBMEC proteome and, in this way, affect BBB dysfunction and the development of HIV-1 CNS disease... - Phosphorylation of claudin-5 and occludin by rho kinase in brain endothelial cellsMasaru Yamamoto
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198 5880, USA
Am J Pathol 172:521-33. 2008..Our results demonstrated the direct phosphorylation of occludin and claudin-5 by RhoK at specific sites, which was increased in encephalitic brain tissue. These antibodies could be useful reagents for monitoring BBB dysfunction in vivo... - Inhibition of indoleamine 2,3-dioxygenase (IDO) enhances elimination of virus-infected macrophages in an animal model of HIV-1 encephalitisRaghava Potula
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology/Experimental Neurosciences, University of Nebraska Medical Center, Omaha, NE 68198-5215, USA
Blood 106:2382-90. 2005..Thus, manipulation of immunosuppressive IDO activity in HIVE may enhance the generation of HIV-1-specific CTLs, leading to elimination of HIV-1-infected macrophages in brain... - HIV-1 activates proinflammatory and interferon-inducible genes in human brain microvascular endothelial cells: putative mechanisms of blood-brain barrier dysfunctionAnathbandhu Chaudhuri
Department of Pharmacology and Experimental Neuroscience, Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, Nebraska 68198 5215, USA
J Cereb Blood Flow Metab 28:697-711. 2008..Analysis of molecular networks and canonical pathways associated with differentially expressed genes suggest that HIV-1 causes BBB impairment by mechanisms involving inflammation, cytokine, and IFN signaling in HBMEC... - Impaired spatial cognition and synaptic potentiation in a murine model of human immunodeficiency virus type 1 encephalitisWalter E Zink
Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, Nebraska 68198-5215, USA
J Neurosci 22:2096-105. 2002..Importantly, the findings demonstrate the value of the model in exploring the physiological basis and therapeutic potential for HIV-1-associated dementia... - Regulation of tissue inhibitor of metalloproteinase-1 by astrocytes: links to HIV-1 dementiaRadhika Suryadevara
Laboratory of Cellular Neuroimmunology, Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA
Glia 44:47-56. 2003..Our studies reveal new opportunities for repair-based therapeutic strategies in HAD... - Alcohol and HIV decrease proteasome and immunoproteasome function in macrophages: implications for impaired immune function during diseaseJames Haorah
Liver Study Unit, The Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, NE 68198-5215, USA
Cell Immunol 229:139-48. 2004..The latter was restored by anti-oxidant. The data support the notion that HIV-1 infection and EtOH may work in concert to affect immune function including antigen presentation and thereby affect disease progression... - Levels of human immunodeficiency virus type 1 (HIV-1) replication in macrophages determines the severity of murine HIV-1 encephalitisAdeline Nukuna
Center for Neurovirology and Neurodegenerative Disorders, Omahan NE 68195-5215, USA
J Neurovirol 10:82-90. 2004..Virus infection, per se, may affect the ability of macrophages to respond to immune stimuli by overproduction of proinflammatory factors and neurotoxins, leading to neuronal dysfunction... - Generation of cytotoxic T cells against virus-infected human brain macrophages in a murine model of HIV-1 encephalitisLarisa Y Poluektova
Center for Neurovirology and Neurodegenerative Disorders, and Department of Pathology, University of Nebraska Medical Center, Omaha, NE 68198, USA
J Immunol 168:3941-9. 2002..The human PBL-NOD-SCID HIVE mouse provides a new tool for studies of cellular immune responses against HIV-1-infected brain mononuclear phagocytes during natural disease and after vaccination... - Mechanism of alcohol-induced oxidative stress and neuronal injuryJames Haorah
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198 5215, USA
Free Radic Biol Med 45:1542-50. 2008..Novel quantitative methods of ROS and NO detection help dissect the mechanisms of alcohol-induced neurodegeneration. Uncovering the basic mechanisms of oxidative neuronal injury will serve as the basis for development of new therapies... - Monocyte chemotactic protein-1 regulates voltage-gated K+ channels and macrophage transmigrationHoward E Gendelman
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology, University of Nebraska Medical Center, Nebraska Medical Center, Omaha, NE 68198 5880, USA
J Neuroimmune Pharmacol 4:47-59. 2009..Together these data demonstrated that MCP-1 affects macrophage migratory movement through regulation of voltage-gated K+ channels and, as such, provides a novel therapeutic strategy for neuroAIDS... - STAT1 signaling modulates HIV-1-induced inflammatory responses and leukocyte transmigration across the blood-brain barrierAnathbandhu Chaudhuri
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198 5215, USA
Blood 111:2062-72. 2008..Inhibition of STAT1 activation could provide a unique therapeutic strategy to attenuate HIV-1-induced BBB compromise and as such improve clinical outcomes... - Peroxisome proliferator-activated receptor-gamma activation suppresses HIV-1 replication in an animal model of encephalitisRaghava Potula
Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, Nebraska, USA
AIDS 22:1539-49. 2008..As PPARgamma agonists are rapidly absorbed by oral administration and efficiently permeate the blood-brain barrier, we hypothesized that PPARgamma stimulation may suppress HIV-1 replication... - Activation of peroxisome proliferator-activated receptor gamma (PPARgamma) suppresses Rho GTPases in human brain microvascular endothelial cells and inhibits adhesion and transendothelial migration of HIV-1 infected monocytesServio H Ramirez
Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha 68198, USA
J Immunol 180:1854-65. 2008..These findings indicate that Rac1 and RhoA inhibition by PPARgamma agonists could be a new approach for treatment of neuroinflammation by preventing monocyte migration across the BBB... - Activation of protein tyrosine kinases and matrix metalloproteinases causes blood-brain barrier injury: Novel mechanism for neurodegeneration associated with alcohol abuseJames Haorah
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska 68198 5215, USA
Glia 56:78-88. 2008..These results provide better understanding of multifaceted effects of alcohol on the brain and could help develop new therapeutic interventions... - Development of a rapid autopsy program for studies of brain immunityAnuja Ghorpade
Laboratory of Cellular Neuroimmunology, 985215 Nebraska Medical Center, Omaha, NE, 68198 5215, USA
J Neuroimmunol 163:135-44. 2005..The challenges in developing this initiative, reflecting experiences from 69 autopsies over 4 years, are presented... - Oxidative stress activates protein tyrosine kinase and matrix metalloproteinases leading to blood-brain barrier dysfunctionJames Haorah
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska 68198 5215, USA
J Neurochem 101:566-76. 2007..These findings point to new therapeutic interventions ameliorating BBB dysfunction in neurological disorders such as stroke or neuroinflammation... - Alcohol-induced blood-brain barrier dysfunction is mediated via inositol 1,4,5-triphosphate receptor (IP3R)-gated intracellular calcium releaseJames Haorah
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska 68198 5215, USA
J Neurochem 100:324-36. 2007..These putative events can lead to BBB dysfunction in the setting of alcoholism, and to neuro-inflammatory disorders promoting leukocyte migration across the BBB... - Novel delivery system enhances efficacy of antiretroviral therapy in animal model for HIV-1 encephalitisTimothy J Spitzenberger
Department of Pharmaceutical Sciences, University of Nebraska Medical Center, Omaha, Nebraska, USA
J Cereb Blood Flow Metab 27:1033-42. 2007..Our findings indicate major antiretroviral effects of P85 and enhanced in vivo efficacy of antiretroviral drugs when combined with P85 in a SCID mouse model of HIVE... - HIV-1 gp120 compromises blood-brain barrier integrity and enhances monocyte migration across blood-brain barrier: implication for viral neuropathogenesisGeorgette D Kanmogne
Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA
J Cereb Blood Flow Metab 27:123-34. 2007..Thus, gp120 can cause dysfunction of BBB via PKC pathways and receptor mediated [Ca(2+)](i) release leading to cytoskeletal alterations and increased monocyte migration... - Inhibition of long-term potentiation by interleukin-8: implications for human immunodeficiency virus-1-associated dementiaHuangui Xiong
The Laboratory of Neurophysiology, Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, Nebraska 68198 5215, USA
J Neurosci Res 71:600-7. 2003..The induction of IL-8 in HAD, its inhibition of LTP, and the expression of its receptor, CXCR2, in the hippocampus all suggest that it plays a role in the cognitive dysfunction associated with HAD... - Infections of the nervous systemHoward E Gendelman
Center for Neurovirology and Neurodegenerative Disorders and Department of Pharmacology, University of Nebraska Medical Center, Omaha NE, USA
Lancet Neurol 4:12-3. 2005 - TNF-related apoptosis-inducing ligand mediates human neuronal apoptosis: links to HIV-1-associated dementiaLisa A Ryan
Laboratory of Neurotoxicology, University of Nebraska Medical Center, Omaha, NE 68195-5215, USA
J Neuroimmunol 148:127-39. 2004..Furthermore, TRAIL induced a dose-dependent effect on neuronal apoptosis. These results support a role for TRAIL in mononuclear phagocyte (MP)-mediated neurotoxicity in HIV-1-associated dementia (HAD)... - T cell independent mechanism for copolymer-1-induced neuroprotectionJianuo Liu
Laboratory of Neuro Immune Regulation, University of Nebraska Medical Center, Omaha, Nebraska, USA
Eur J Immunol 37:3143-54. 2007..These findings may facilitate the development of neuroprotective approaches using DC-mediated Cop-1 delivery to diseased nervous tissue... - Blocking TNF-alpha attenuates aneurysm formation in a murine modelWanfen Xiong
Department of Surgery, University of Nebraska Medical Center, Omaha, NE 68198, USA
J Immunol 183:2741-6. 2009..This study confirms that a strategy of TNF-alpha antagonism may be an important therapeutic strategy for treating AAA... - Adding fuel to the fire: methamphetamine enhances HIV infectionRaghava Potula
Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198-5215, USA
Am J Pathol 172:1467-70. 2008
Research Grants
- Effect of Alcohol on HIV-1 Immune Responses & BBB DamageYuri Persidsky; Fiscal Year: 2004..The ability to use an in vitro BBB and an in vivo animal model will help in defining mechanisms of disease progression in the setting of alcohol abuse. ..