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GM-CSF regulates alveolar macrophage differentiation and innate immunity in the lung through PU.1

Y Shibata1, P Y Berclaz, Z C Chroneos

  • 1Division of Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, OH 45229, USA.

Immunity
|October 24, 2001
PubMed

Insights

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is crucial for lung immunity. PU.1 transcription factor restores innate immune functions and surfactant catabolism in alveolar macrophages.

Area of Science:

  • Immunology
  • Pulmonary Medicine
  • Cell Biology

Background:

  • GM-CSF gene targeted (GM(-/-)) mice exhibit susceptibility to respiratory infections.
  • GM(-/-) mice develop alveolar proteinosis due to impaired innate immune function and surfactant catabolism in alveolar macrophages (AMs).
  • AMs from GM(-/-) mice show reduced cell adhesion, phagocytosis, pathogen killing, and receptor expression.

Purpose of the Study:

  • To investigate the role of PU.1 transcription factor in GM-CSF-dependent regulation of AM function.
  • To determine if PU.1 can restore innate immune functions and surfactant catabolism in GM(-/-) mice.

Main Methods:

  • Analysis of AMs from GM(-/-) mice and SPC-GM/GM(-/-) transgenic mice.
  • Assessment of innate immune functions and surfactant catabolism in AMs.
  • Retrovirus-mediated expression of PU.1 in AMs from GM(-/-) mice.

Main Results:

  • PU.1 levels were markedly reduced in AMs of GM(-/-) mice.
  • Selective expression of GM-CSF in the lungs of SPC-GM/GM(-/-) transgenic mice restored PU.1.
  • Retrovirus-mediated PU.1 expression rescued host defense and surfactant catabolism in GM(-/-) AMs.

Conclusions:

  • PU.1 is a critical mediator of GM-CSF-dependent effects on AM terminal differentiation.
  • PU.1 regulates innate immune functions and surfactant catabolism by AMs.
  • Targeting PU.1 may offer therapeutic potential for respiratory infections and alveolar proteinosis.

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