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

Research output: Contribution to journalArticlepeer-review

74 Scopus citations


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
Issue number1-2
StatePublished - May 2003


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

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology


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