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Airway hyperresponsiveness is dissociated from airway wall structural remodeling
Salman Siddiqui1, Vijay Mistry, Camille Doe
1Institute of Lung Health, Leicester, United Kingdom.
The Journal of Allergy and Clinical Immunology
|June 24, 2008
Summary
Nonasthmatic eosinophilic bronchitis (EB) and asthma show increased airway smooth muscle mass and reticular basement membrane thickness. Mast cell presence in airway smooth muscle, not airway wall remodeling, is linked to airway hyperresponsiveness (AHR).
Area of Science:
- Pulmonary Medicine
- Respiratory Research
- Airway Inflammation
Background:
- Nonasthmatic eosinophilic bronchitis (EB) is a model for studying airway hyperresponsiveness (AHR).
- Previous studies showed vascular remodeling and reticular basement membrane (RBM) thickening in EB.
- The presence of other structural remodeling features in EB remained unknown.
Purpose of the Study:
- To investigate structural remodeling in EB.
- To determine if structural remodeling in EB is associated with AHR and airflow limitation.
Main Methods:
- Compared airway biopsy samples from patients with asthma, EB, and healthy volunteers.
- Assessed airway smooth muscle (ASM) area, RBM thickness, collagen 3 deposition, glandular area, mast cells, and granulocytes.
- Analyzed associations between structural remodeling features and AHR.
Main Results:
- Both EB and asthma showed increased ASM mass and RBM thickness compared to healthy subjects.
- No significant differences in collagen 3 deposition or glandular area were found.
- Mast cell numbers within the ASM were the only remodeling feature associated with AHR.
Conclusions:
- Mast cell localization to the ASM bundle is associated with AHR in asthma.
- Structural remodeling of the airway wall itself is not directly associated with AHR in this study.
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