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How does airway inflammation modulate asthmatic airway constriction? An antigen challenge study
A C Henderson1, E P Ingenito, H Atileh
1Department of Biomedical Engineering, Boston University, Boston, MA 02215, USA.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|April 22, 2003
Summary
Asthma attacks involve airway inflammation and constriction. This study found that while inflammation is common in the late-phase response, airway constriction varies, suggesting differences in smooth muscle response contribute to asthma severity.
Area of Science:
- Pulmonary Medicine
- Allergy and Immunology
- Respiratory Physiology
Background:
- The late-phase (LP) response to inhaled allergens in asthma involves airway inflammation, similar to asthma attacks.
- Deep inspiration (DI) can affect airway caliber and reversibility of bronchoconstriction.
Purpose of the Study:
- To compare airway obstruction and bronchodilator reversibility during early-phase (EP) and LP allergic responses in asthmatic subjects.
- To investigate the relationship between airway inflammation and the pattern of airway constriction during allergic responses.
Main Methods:
- Assessed heterogeneity of airway constriction using frequency dependence of dynamic lung resistance and elastance.
- Measured airway caliber changes during DI and airway inflammation via induced sputum analysis.
- Compared EP and LP responses to allergen challenge in nine asthmatic subjects.
Main Results:
- Asthmatic subjects exhibited significant EP response with heterogeneous constriction and reduced maximal airway dilation capacity.
- LP response was associated with airway inflammation in all subjects, but constriction severity varied.
- Four subjects showed marked LP constriction similar to EP, while five had mild LP constriction.
- Bronchoconstriction during LP was fully reversible with bronchodilators.
- Impaired bronchodilatory response during DI was observed.
Conclusions:
- Airway inflammation in asthma is linked to a nonuniform pattern of airway constriction.
- Variability in asthma responsiveness may stem from intrinsic differences in smooth muscle response to inflammation.
- Physiological abnormalities at the smooth muscle level contribute to asthma pathology.
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