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Differential expression of interferon alpha and beta induced with Newcastle disease virus in mouse macrophage

A Hoss1, E C Zwarthoff, R Zawatzky

  • 1Institute of Virus Research, German Cancer Research Center, Heidelberg.

Insights

Newcastle disease virus (NDV) triggers a strong interferon (IFN) response in mouse macrophages. Macrophage colony-stimulating factor 1 (M-CSF) significantly boosts IFN production, particularly IFN-alpha, in cultured macrophages.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Newcastle disease virus (NDV) induces a robust interferon (IFN) response in macrophages.
  • Mouse genotype influences the magnitude of this IFN response.
  • Previous studies suggest macrophage activation status impacts IFN production.

Purpose of the Study:

  • To investigate the effect of macrophage colony-stimulating factor 1 (M-CSF) on NDV-induced IFN production in vitro.
  • To compare IFN production at protein and mRNA levels in different macrophage populations.
  • To elucidate the role of M-CSF in regulating IFN-alpha and IFN-beta gene expression.

Main Methods:

  • Primary macrophages were derived from C57BL/6 ('high producer') and BALB/c ('low producer') mice.
  • Macrophages were cultured with or without L cell conditioned medium (CM) or purified murine M-CSF.
  • NDV stimulation was used to induce IFN production.
  • IFN protein levels were measured using specific monoclonal antibodies.
  • IFN mRNA levels were analyzed using hybridization experiments with DNA probes.

Main Results:

  • Macrophages cultured with CM or M-CSF produced 10- to 50-fold more IFN per cell than resident peritoneal macrophages.
  • This enhancement was observed at both protein and mRNA levels.
  • CM- or M-CSF-cultured macrophages produced both IFN-alpha and IFN-beta, while resident macrophages produced almost exclusively IFN-beta.
  • M-CSF significantly increased IFN-alpha gene expression.

Conclusions:

  • M-CSF significantly enhances NDV-induced IFN synthesis in mouse macrophages.
  • This enhancement is partly due to M-CSF's ability to activate IFN-alpha gene expression.
  • Macrophage activation status, influenced by M-CSF, plays a critical role in determining the type and quantity of IFN produced.

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