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Fluticasone Induces Epithelial Injury and Alters Barrier Function in Normal Subjects.
Ruth E MacRedmond1, Gurpreet K Singhera1, Samuel J Wadsworth1
1Centre for Heart Lung Innovation, St. Paul's Hospital, University of British Columbia, Vancouver, Canada.
Journal of Steroids & Hormonal Science
|October 18, 2014
Summary
Inhaled corticosteroids may injure the airway epithelium, increasing epithelial cells in sputum. This response, though potentially protective, requires further study in asthma patients to understand airway remodeling.
Area of Science:
- Respiratory Medicine
- Cell Biology
- Pharmacology
Background:
- The airway epithelium acts as a critical barrier against inhaled substances.
- Asthma pathogenesis involves impaired epithelial integrity due to dysregulated injury and repair.
- Inhaled corticosteroids (ICS) are standard asthma therapy but do not prevent airway remodeling.
Purpose of the Study:
- To investigate the direct effects of inhaled fluticasone on normal human airway epithelium.
- To assess the impact of ICS on epithelial integrity, inflammation, and barrier function.
Main Methods:
- Healthy subjects received inhaled fluticasone (500 μg BID) for 4 weeks.
- Induced sputum analyzed for cell counts and inflammatory markers.
- Airway barrier function assessed via diethylenetriaminepentacetic acid (DTPA) clearance and sputum albumin levels.
Main Results:
- Fluticasone treatment significantly increased airway epithelial cells in sputum, indicating injury.
- No significant changes observed in sputum inflammatory cell counts or cytokine levels.
- Epithelial shedding correlated with improved barrier function (decreased DTPA clearance, reduced sputum albumin), suggesting a repair response.
Conclusions:
- Inhaled corticosteroids can induce injury in normal airway epithelium.
- These findings suggest ICS-induced epithelial injury may play a role in asthma, potentially contributing to airway remodeling.
- Further research is needed to elucidate these effects in the context of asthma's aberrant repair mechanisms.
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