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

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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 languageEnglish (US)
Pages (from-to)144-155
Number of pages12
JournalJournal of Neuroimmunology
Volume138
Issue number1-2
DOIs
StatePublished - May 2003

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Keywords

  • Chemokines
  • Fractalkine
  • HIV-1 associated dementia
  • Inflammation
  • Macrophage

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

Cite this

Erichsen, D., Lopez, A. L., Peng, H., Niemann, D., Williams, C., Bauer, M., Morgello, S., Cotter, R. L., Ryan, L. A., Ghorpade, A., Gendelman, H. E., & Zheng, J. (2003). Neuronal injury regulates fractalkine: Relevance for HIV-1 associated dementia. Journal of Neuroimmunology, 138(1-2), 144-155. https://doi.org/10.1016/S0165-5728(03)00117-6