Mannitol challenge for assessment of airway responsiveness, airway inflammation and inflammatory phenotype in asthma

Authors

  • L. G. Wood,

    1. Respiratory and Sleep Medicine, Hunter Medical Research Institute, John Hunter Hospital, New Lambton, NSW, Australia
    2. Centre for Asthma and Respiratory Disease, University of Newcastle, Newcastle, NSW, Australia
    3. Asthma and Airways Cooperative Research Centre, Sydney, NSW, Australia
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  • H. Powell,

    1. Respiratory and Sleep Medicine, Hunter Medical Research Institute, John Hunter Hospital, New Lambton, NSW, Australia
    2. Centre for Asthma and Respiratory Disease, University of Newcastle, Newcastle, NSW, Australia
    3. Asthma and Airways Cooperative Research Centre, Sydney, NSW, Australia
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  • P. G. Gibson

    1. Respiratory and Sleep Medicine, Hunter Medical Research Institute, John Hunter Hospital, New Lambton, NSW, Australia
    2. Centre for Asthma and Respiratory Disease, University of Newcastle, Newcastle, NSW, Australia
    3. Asthma and Airways Cooperative Research Centre, Sydney, NSW, Australia
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Correspondence:
Dr Lisa G. Wood, Respiratory and Sleep Medicine, Level 3, Hunter Medical Research Institute, John Hunter Hospital, Newcastle, NSW, Australia.
E-mail: lisa.wood@newcastle.edu.au

Summary

Background Assessment of airway inflammation in asthma is becoming increasingly important, as the inflammatory phenotype underpins the treatment response.

Objective This study aimed to evaluate mannitol as a tool for assessing airway responsiveness and airway inflammation in asthma, compared with hypertonic saline.

Methods Fifty-five subjects with stable asthma completed a hypertonic (4.5%) saline challenge and a mannitol challenge at two separate visits, performed 48–72 h apart, in random order.

Results Induced sputum was obtained from 49 (89%) subjects during the saline challenge and 42 (76%) subjects during the mannitol challenge (P>0.05). There was a significant correlation between the greatest percentage fall in forced expiratory volume in 1 s (FEV1) (r=0.6, P<0.0001), the dose–response slope (r=0.73), cumulative dose (r=0.55) and PD15 (r=0.46) for mannitol and hypertonic saline. The greatest percentage fall in FEV1 to mannitol was less in non-eosinophilic asthma. There was a lower total cell count in mannitol vs. hypertonic-saline-induced sputum. However, sputum eosinophils and neutrophils were not significantly different. Using mannitol, a higher proportion of subjects were classified as having eosinophilic asthma. There were no differences in IL-8, neutrophil elastase or matrix-metalloproteinase 9 concentrations in sputum samples induced with mannitol or hypertonic saline.

Conclusion We conclude that mannitol can be used to induce good-quality sputum, useful for analysis of inflammatory mediators and for predicting the inflammatory phenotype in asthma.

Cite this as: L. G. Wood, H. Powell and P. G. Gibson, Clinical & Experimental Allergy, 2010 (40) 232–241.

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