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p47phox deficiency induces macrophage dysfunction resulting in progressive crystalline macrophage pneumonia

Qi Liu1, Lily I Cheng, Liang Yi

  • 1Monocyte Trafficking Unit, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-1456, USA.

The American Journal of Pathology
|December 20, 2008
PubMed

Insights

Nicotinamide dinucleotide phosphate oxidase-deficient mice develop crystalline macrophage pneumonia. Their macrophages exhibit pliable activation, suggesting a role in chronic granulomatous disease pathogenesis.

Area of Science:

  • Immunology
  • Pathology
  • Cell Biology

Background:

  • Nicotinamide dinucleotide phosphate oxidase-deficient (p47phox-/-) mice model human chronic granulomatous disease, exhibiting susceptibility to infections and inflammation.
  • Antibiotic prophylaxis in p47phox-/- mice prevents infections, allowing for the study of underlying disease pathology.
  • These mice develop proliferative macrophage lesions containing Ym1/Ym2 protein and crystals in multiple organs.

Purpose of the Study:

  • To investigate the progression and characteristics of macrophage lesions in infection-free p47phox-/- mice.
  • To determine the cytokine profiles associated with macrophage activation in these mice.
  • To explore the functional plasticity of macrophages in the context of p47phox-/- dysfunction.

Main Methods:

  • Histological examination of lung, bone marrow, lymph nodes, and spleen from p47phox-/- mice.
  • Analysis of Ym1/Ym2 protein and crystal presence within macrophages.
  • Measurement of Th-1, Th-2, Th-17, and interleukin-12 cytokine levels in bronchoalveolar lavage fluid.

Main Results:

  • Lung lesions progressed from localized crystalline macrophage accumulation to diffuse crystalline macrophage pneumonia without fibrosis.
  • Ym1/Ym2 protein crystals were observed within macrophages in various tissues.
  • Elevated levels of interferon-gamma, interleukin-4, interleukin-17, and interleukin-12 were detected, indicating mixed macrophage activation phenotypes.

Conclusions:

  • p47phox-/- macrophages display remarkable functional plasticity, capable of adopting both classical and alternative activation phenotypes.
  • This macrophage pliability is linked to intrinsic defects in their activation pathways.
  • The findings provide insights into the pathogenesis of inflammatory diseases in p47phox-/- mice and potentially in chronic granulomatous disease.

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