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Osteopontin prevents monocyte recirculation and apoptosis

Tricia H Burdo1, Malcolm R Wood, Howard S Fox

  • 1Molecular and Integrative Neurosciences Department, The Scripps Research Institute, 10550 North Torrey Pines Rd., SP30-2030, La Jolla, CA 92037, USA.

Journal of Leukocyte Biology
|March 21, 2007
PubMed

Insights

Osteopontin (OPN) promotes macrophage accumulation in the brain during HIV-1 infection by preventing cell recirculation and apoptosis. This contributes to the pathology of HIV-1-associated dementia (HAD).

Area of Science:

  • Neuroimmunology
  • Virology
  • Cell Biology

Background:

  • Monocyte/macrophage lineage cells are primary targets for HIV-1 replication in the central nervous system (CNS).
  • HIV-1-associated dementia (HAD) correlates with increased macrophage presence in the brain.
  • Mechanisms preventing macrophage exit from the brain and promoting survival may contribute to their accumulation.

Purpose of the Study:

  • To investigate the role of osteopontin (OPN) in the accumulation of macrophages within the brain during neuroAIDS.
  • To elucidate OPN's contribution to macrophage survival and accumulation in the context of HAD pathogenesis.

Main Methods:

  • Utilized in vitro model systems to study OPN's effects on macrophages.
  • Assessed OPN's influence on macrophage recirculation and apoptosis.

Main Results:

  • Osteopontin (OPN) was demonstrated to prevent macrophage recirculation from the brain.
  • OPN was shown to protect macrophages from undergoing apoptosis.
  • These actions of OPN contribute to macrophage survival and accumulation in the CNS.

Conclusions:

  • Osteopontin (OPN) plays a significant role in the accumulation of macrophages in the brain during HIV-1 infection.
  • OPN's dual action of preventing egress and apoptosis supports macrophage persistence, contributing to the neuropathology of HAD.
  • Targeting OPN may offer a therapeutic strategy for managing neuroAIDS and HAD.

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