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GM-CSF increases AP-1 DNA binding and Ref-1 amounts in human alveolar macrophages
D M Flaherty1, M M Monick, A B Carter
1Department of Internal Medicine, University of Iowa College of Medicine and Veterans Administration Medical Center, Iowa City, Iowa 52242, USA. flahertydm@mail.medicine.uiowa.edu
American Journal of Respiratory Cell and Molecular Biology
|August 18, 2001
Summary
Chronic lung disease alters alveolar macrophages, decreasing activator protein (AP)-1 DNA binding. Granulocyte-macrophage colony-stimulating factor (GM-CSF) can restore AP-1 activity, suggesting a role in disease pathogenesis.
Area of Science:
- Pulmonary immunology
- Cellular biology
- Molecular mechanisms of lung disease
Background:
- Alveolar macrophages are key in lung disorders.
- Chronic lung diseases alter macrophage phenotype towards monocyte-like cells.
- Normal alveolar macrophages show reduced activator protein (AP)-1 DNA binding due to impaired redox regulation via Ref-1.
Purpose of the Study:
- To investigate if factors in chronic lung disease increase AP-1 DNA binding and Ref-1 in alveolar macrophages.
- To examine the role of granulocyte-macrophage colony-stimulating factor (GM-CSF) as a potential mediator.
Main Methods:
- Incubation of human alveolar macrophages with GM-CSF for 24 hours.
- Assessment of AP-1 DNA binding activity.
- Western blot analysis for Ref-1 protein levels.
- Stimulation with interleukin (IL)-13 and phorbol myristate acetate (PMA).
Main Results:
- GM-CSF significantly increased AP-1 DNA binding in unstimulated, IL-13, and PMA-stimulated alveolar macrophages.
- A corresponding increase in Ref-1 protein was observed in PMA-stimulated cells.
- GM-CSF and IL-13 may modulate AP-1 DNA binding activity in alveolar macrophages.
Conclusions:
- Disease-related cytokines like GM-CSF and IL-13 can enhance AP-1 DNA binding in alveolar macrophages.
- This modulation of AP-1 activity by GM-CSF suggests its involvement in the fibrotic processes of chronic lung disease.
- Understanding these mechanisms is crucial for targeting lung disease pathogenesis.
