Mannitol and AMP do not induce bronchoconstriction in eosinophilic bronchitis: Further evidence for dissociation between airway inflammation and bronchial hyperresponsiveness
Article first published online: 24 FEB 2010
© 2010 The Authors. Journal compilation © 2010 Asian Pacific Society of Respirology
Volume 15, Issue 3, pages 510–515, April 2010
How to Cite
SINGAPURI, A., MCKENNA, S., BRIGHTLING, C. E. and BRADDING, P. (2010), Mannitol and AMP do not induce bronchoconstriction in eosinophilic bronchitis: Further evidence for dissociation between airway inflammation and bronchial hyperresponsiveness. Respirology, 15: 510–515. doi: 10.1111/j.1440-1843.2010.01712.x
- Issue published online: 29 MAR 2010
- Article first published online: 24 FEB 2010
- Received 2 September 2009; invited to revise 5 October 2009; revised 14 October 2009; accepted 15 November 2009 (Associate Editor: Robin Taylor).
- eosinophilic bronchitis;
- airway hyperresponsiveness;
- adenosine monophosphate
Background and objective: Eosinophilic bronchitis (EB) shares many pathological features with asthma. However, patients with EB do not develop the characteristic physiological abnormalities of asthma: variable airflow obstruction and bronchial hyperresponsiveness (BHR) to a direct bronchial challenge with methacholine. Indirect bronchial challenges with AMP and mannitol are dependent on the presence of airway inflammation, and positive in 10% of asthmatic subjects who have a negative response to methacholine. We have therefore investigated whether subjects with EB are responsive to indirect airway challenge with AMP and mannitol.
Methods: Subjects with asthma, EB and healthy controls attended on up to four occasions. After screening, subjects performed bronchial provocation tests to methacholine and then either AMP or mannitol. Each challenge was followed immediately by sputum induction for the measurement of airway inflammation and mast cell-derived histamine.
Results: No subjects with EB responded to either AMP (n = 5) or mannitol (n = 7) while 4/8 and 7/10 subjects with asthma responded to the respective challenges (P = 0.057 for AMP, P = 0.004 for mannitol). There was no difference in induced sputum concentrations of histamine or eosinophil cell counts following methacholine challenge compared with AMP or mannitol.
Conclusions: The airways of patients with EB are not responsive to either direct or indirect bronchial challenge. This supports the view that it is the presence of functionally abnormal airway smooth muscle that is the key determinant of BHR in asthma, and that while this may be aggravated by the presence of mucosal airway inflammation, it is not caused by it.