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Analysis of Microglia and Monocyte-derived Macrophages from the Central Nervous System by Flow Cytometry
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Ly6c+ "inflammatory monocytes" are microglial precursors recruited in a pathogenic manner in West Nile virus

Daniel R Getts1, Rachael L Terry, Meghann Teague Getts

  • 1The Discipline of Pathology, School of Medical Sciences, The University of Sydney, Sydney NSW 2006, Australia.

The Journal of Experimental Medicine
|September 10, 2008
PubMed

Insights

Inflammatory monocytes migrate to the brain during West Nile virus (WNV) infection, becoming new microglia. Blocking the CCL2 chemokine reduces this influx and improves survival in WNV encephalitis models.

Area of Science:

  • Neuroimmunology
  • Virology
  • Infectious Diseases

Background:

  • Central nervous system (CNS) infections, such as West Nile virus (WNV), can lead to significant neuroinflammation.
  • Microglia, the resident immune cells of the brain, play a crucial role in the response to CNS pathogens.
  • The origin and expansion of microglia during acute viral encephalitis remain incompletely understood.

Purpose of the Study:

  • To investigate the cellular source of increased microglia during West Nile virus (WNV) infection.
  • To determine the role of monocytes in replenishing microglia populations in the infected brain.
  • To explore the therapeutic potential of targeting monocyte recruitment in WNV encephalitis.

Main Methods:

  • Utilized a lethal West Nile virus (WNV) mouse model.
  • Employed flow cytometry and genetic labeling (EGFP bone marrow chimeras) to track cell populations.
  • Performed monocyte depletion studies and adoptive transfer experiments.
  • Investigated the role of the chemokine CCL2 through neutralization assays.

Main Results:

  • WNV infection led to a threefold increase in microglia, with few cells proliferating, indicating peripheral origin.
  • Depletion of classical monocytes abrogated the microglial expansion.
  • Peripherally derived monocytes were identified as microglial precursors in the infected brain.
  • CCL2 neutralization reduced microglial infiltration and prolonged survival in WNV-infected animals.

Conclusions:

  • Inflammatory monocytes are a critical source of microglia during West Nile virus (WNV) infection.
  • CCL2-dependent monocyte recruitment to the brain contributes to microglial expansion.
  • Targeting CCL2-mediated monocyte migration offers a potential therapeutic strategy for WNV encephalitis.

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