Neuronal injury regulates fractalkine: Relevance for HIV-1 associated dementia

David Erichsen; Alicia L. Lopez; Hui Peng; Douglas Niemann; Clancy Williams; Michael Bauer; Susan Morgello; Robin L. Cotter; Lisa A. Ryan; Anuja Ghorpade; Howard E. Gendelman; Jialin Zheng

doi:10.1016/S0165-5728(03)00117-6

Neuronal injury regulates fractalkine: Relevance for HIV-1 associated dementia

David Erichsen, Alicia L. Lopez, Hui Peng, Douglas Niemann, Clancy Williams, Michael Bauer, Susan Morgello, Robin L. Cotter, Lisa A. Ryan, Anuja Ghorpade, Howard E. Gendelman, Jialin Zheng

Pharmaceutical Sciences

Research output: Contribution to journal › Article › peer-review

76 Scopus citations

Abstract

Fractalkine (FKN), a chemokine highly expressed in the central nervous system, participates in inflammatory responses operative in many brain disorders including HIV-1 associated dementia (HAD). In this report, HIV-1 progeny virions and pro-inflammatory products led to FKN production associated with neuronal injury and apoptosis. FKN was produced by neurons and astrocytes; but differentially produced by the two cell types. Laboratory tests paralleled those in infected people where cerebrospinal fluid FKN levels in HIV-1 infected cognitively impaired (n=16) patients were found to be increased when compared to infected patients without cognitive impairment (n=8, P=0.0345). These results demonstrate a possible role of FKN in HAD pathogenesis.

Original language	English
Pages (from-to)	144-155
Number of pages	12
Journal	Journal of Neuroimmunology
Volume	138
Issue number	1-2
DOIs	https://doi.org/10.1016/S0165-5728(03)00117-6
State	Published - May 2003

Bibliographical note

Funding Information:
This work was supported in part by National Institutes of Health research grants: R01 NS 41858-01 (to JZ) and P20 RR15635-01 (to JZ and HEG).

Funding Information:
We kindly thank Manhattan HIV Brain Bank for providing the cerebrospinal fluid samples from HIV-1 infected subjects which is currently supported by NIH (R24MH59724); Ms. Robin Shepard for critically reading this manuscript; Ms. Li Wu and Ms. Lesley Gendelman for technical support; and Ms. Julie Ditter, Ms. Robin Taylor, Ms. Theresa Grutel and Ms. Nellie Ingraham for outstanding administrative support.

Keywords

Chemokines
Fractalkine
HIV-1 associated dementia
Inflammation
Macrophage

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/S0165-5728(03)00117-6

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title = "Neuronal injury regulates fractalkine: Relevance for HIV-1 associated dementia",

abstract = "Fractalkine (FKN), a chemokine highly expressed in the central nervous system, participates in inflammatory responses operative in many brain disorders including HIV-1 associated dementia (HAD). In this report, HIV-1 progeny virions and pro-inflammatory products led to FKN production associated with neuronal injury and apoptosis. FKN was produced by neurons and astrocytes; but differentially produced by the two cell types. Laboratory tests paralleled those in infected people where cerebrospinal fluid FKN levels in HIV-1 infected cognitively impaired (n=16) patients were found to be increased when compared to infected patients without cognitive impairment (n=8, P=0.0345). These results demonstrate a possible role of FKN in HAD pathogenesis.",

keywords = "Chemokines, Fractalkine, HIV-1 associated dementia, Inflammation, Macrophage",

author = "David Erichsen and Lopez, {Alicia L.} and Hui Peng and Douglas Niemann and Clancy Williams and Michael Bauer and Susan Morgello and Cotter, {Robin L.} and Ryan, {Lisa A.} and Anuja Ghorpade and Gendelman, {Howard E.} and Jialin Zheng",

note = "Funding Information: This work was supported in part by National Institutes of Health research grants: R01 NS 41858-01 (to JZ) and P20 RR15635-01 (to JZ and HEG). Funding Information: We kindly thank Manhattan HIV Brain Bank for providing the cerebrospinal fluid samples from HIV-1 infected subjects which is currently supported by NIH (R24MH59724); Ms. Robin Shepard for critically reading this manuscript; Ms. Li Wu and Ms. Lesley Gendelman for technical support; and Ms. Julie Ditter, Ms. Robin Taylor, Ms. Theresa Grutel and Ms. Nellie Ingraham for outstanding administrative support. ",

year = "2003",

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doi = "10.1016/S0165-5728(03)00117-6",

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T2 - Relevance for HIV-1 associated dementia

AU - Erichsen, David

AU - Lopez, Alicia L.

AU - Peng, Hui

AU - Niemann, Douglas

AU - Williams, Clancy

AU - Bauer, Michael

AU - Morgello, Susan

AU - Cotter, Robin L.

AU - Ryan, Lisa A.

AU - Ghorpade, Anuja

AU - Gendelman, Howard E.

AU - Zheng, Jialin

N1 - Funding Information: This work was supported in part by National Institutes of Health research grants: R01 NS 41858-01 (to JZ) and P20 RR15635-01 (to JZ and HEG). Funding Information: We kindly thank Manhattan HIV Brain Bank for providing the cerebrospinal fluid samples from HIV-1 infected subjects which is currently supported by NIH (R24MH59724); Ms. Robin Shepard for critically reading this manuscript; Ms. Li Wu and Ms. Lesley Gendelman for technical support; and Ms. Julie Ditter, Ms. Robin Taylor, Ms. Theresa Grutel and Ms. Nellie Ingraham for outstanding administrative support.

PY - 2003/5

Y1 - 2003/5

N2 - Fractalkine (FKN), a chemokine highly expressed in the central nervous system, participates in inflammatory responses operative in many brain disorders including HIV-1 associated dementia (HAD). In this report, HIV-1 progeny virions and pro-inflammatory products led to FKN production associated with neuronal injury and apoptosis. FKN was produced by neurons and astrocytes; but differentially produced by the two cell types. Laboratory tests paralleled those in infected people where cerebrospinal fluid FKN levels in HIV-1 infected cognitively impaired (n=16) patients were found to be increased when compared to infected patients without cognitive impairment (n=8, P=0.0345). These results demonstrate a possible role of FKN in HAD pathogenesis.

AB - Fractalkine (FKN), a chemokine highly expressed in the central nervous system, participates in inflammatory responses operative in many brain disorders including HIV-1 associated dementia (HAD). In this report, HIV-1 progeny virions and pro-inflammatory products led to FKN production associated with neuronal injury and apoptosis. FKN was produced by neurons and astrocytes; but differentially produced by the two cell types. Laboratory tests paralleled those in infected people where cerebrospinal fluid FKN levels in HIV-1 infected cognitively impaired (n=16) patients were found to be increased when compared to infected patients without cognitive impairment (n=8, P=0.0345). These results demonstrate a possible role of FKN in HAD pathogenesis.

KW - Chemokines

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KW - Inflammation

KW - Macrophage

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Neuronal injury regulates fractalkine: Relevance for HIV-1 associated dementia

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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