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Autocrine activation of cultured macrophages by brain-derived neurotrophic factor

Toshio Asami1, Takuya Ito, Hidefumi Fukumitsu

  • 1Laboratory of Molecular Biology, Gifu Pharmaceutical University, 5-6-1, Mitahora-Higashi, Gifu 502-8585, Japan.

Biochemical and Biophysical Research Communications
|April 25, 2006
PubMed

Insights

Brain-derived neurotrophic factor (BDNF) enhances macrophage phagocytosis and interleukin-1beta secretion, suggesting BDNF plays a key role in macrophage activation via autocrine signaling.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Activated microglia/macrophages are crucial in central nervous system injury.
  • The role of brain-derived neurotrophic factor (BDNF) in these cells is not fully understood.

Purpose of the Study:

  • To investigate the significance of BDNF expression in activated microglia/macrophages.
  • To examine BDNF's actions on and synthesis by macrophages.

Main Methods:

  • Cultured macrophages from mouse peritoneal cavity.
  • Assessed BDNF and neurotrophin-3 (NT-3) synthesis.
  • Measured expression of TrkB (full-length and truncated) and TrkC receptors.
  • Evaluated phagocytic activity and interleukin-1beta secretion.

Main Results:

  • Macrophages synthesized BDNF and NT-3, expressing TrkB and TrkC receptors, indicating autocrine signaling.
  • BDNF, not NT-3, enhanced macrophage phagocytosis and interleukin-1beta secretion, similar to lipopolysaccharide (LPS).
  • Phagocytic activity correlated significantly with BDNF or full-length TrkB (TrkB(FL)) expression.

Conclusions:

  • Macrophage phagocytic activity is dependent on BDNF synthesis and/or TrkB(FL) expression.
  • BDNF likely participates in macrophage activation through autocrine mechanisms.
  • BDNF is a key mediator in the inflammatory response within the injured central nervous system.

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