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Dysregulated apoptosis and NFkappaB expression in COPD subjects
Vanessa Brown1, J Stuart Elborn, Judy Bradley
1Respiratory Research Group, Centre for Infection and Immunity, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, UK. v.brown@qub.ac.uk
Respiratory Research
|March 20, 2009
Summary
Neutrophil apoptosis is reduced in chronic obstructive pulmonary disease (COPD) and smokers, potentially linked to nuclear factor-kappa B (NFkappaB) activation. This finding may explain ineffective inflammation resolution in these conditions.
Area of Science:
- Pulmonary Medicine
- Immunology
- Cell Biology
Background:
- Abnormal neutrophil apoptosis contributes to unresolved inflammation in chronic lung diseases.
- Nuclear factor-kappa B (NFkappaB) signaling delays constitutive neutrophil apoptosis.
- Previous studies suggested airway cell apoptosis dysregulation in COPD, but NFkappaB's role in COPD neutrophils was uninvestigated.
Purpose of the Study:
- To examine spontaneous neutrophil apoptosis in stable COPD subjects, healthy smokers, and non-smoking controls.
- To investigate the association between NFkappaB activation and neutrophil apoptosis in inflammatory conditions.
Main Methods:
- Apoptosis analysis in induced sputum using light microscopy, Annexin V/Propidium iodide, and TUNEL assay.
- NFkappaB activation assessment via flow cytometry.
- IkappaBalpha phosphorylation analysis using the Bio-Rad Bio-Plex assay.
Main Results:
- Reduced spontaneous neutrophil apoptosis in COPD subjects and healthy smokers compared to non-smokers (p < 0.001).
- Similar findings confirmed by TUNEL assay and morphological identification.
- Increased expression of NFkappaB p50 and p65 subunits in neutrophils from COPD subjects (p = 0.006).
Conclusions:
- Neutrophil apoptosis is decreased in the sputum of COPD subjects and healthy smokers.
- This reduction in apoptosis may be regulated by NFkappaB activation.
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