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Delayed eosinophil apoptosis in asthma.
H Kankaanranta1, M A Lindsay, M A Giembycz
1Department of Thoracic Medicine, Imperial College School of Medicine at the National Heart and Lung Institute, London, United Kingdom.
The Journal of Allergy and Clinical Immunology
|July 11, 2000
Summary
Eosinophil apoptosis is delayed in asthma, potentially due to GM-CSF. Beta(2)-agonists may worsen eosinophilia by inhibiting apoptosis, while inhaled glucocorticoids reverse this delay.
Area of Science:
- Immunology
- Respiratory Medicine
- Cell Biology
Background:
- Eosinophilic airway inflammation is a hallmark of asthma.
- Defects in eosinophil apoptosis may contribute to chronic eosinophilia in asthma.
Purpose of the Study:
- To investigate differences in peripheral blood eosinophil apoptosis rates between asthma patients and healthy individuals.
Main Methods:
- Isolated peripheral blood eosinophils from asthma patients and controls.
- Cultured eosinophils for 48 hours and assessed apoptosis via flow cytometry.
- Investigated the role of IL-3, IL-5, GM-CSF, and beta(2)-agonists on eosinophil apoptosis.
Main Results:
- Eosinophils from untreated asthma patients exhibited delayed apoptosis compared to healthy controls.
- Steroid treatment normalized eosinophil apoptosis rates.
- GM-CSF neutralization increased apoptosis; beta(2)-agonists inhibited apoptosis in vitro.
- In vitro exposure to GM-CSF or IL-5 did not prevent apoptosis, but albuterol did.
Conclusions:
- Asthma is associated with delayed eosinophil apoptosis, possibly mediated by GM-CSF.
- Beta(2)-agonist use may prolong eosinophil survival, potentially exacerbating asthma.
- Inhaled glucocorticoids appear to fully reverse the delayed eosinophil apoptosis observed in asthma.
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