Asthma and lower airway diseaseTranscriptional phenotypes of asthma defined by gene expression profiling of induced sputum samples
Section snippets
Participants
Adults with stable asthma were recruited from the John Hunter Hospital Ambulatory Care Clinic, Newcastle, Australia. Asthma was diagnosed according to American Thoracic Society guidelines on the basis of current (past 12 months) episodic respiratory symptoms, doctor’s diagnosis (ever), and demonstrated evidence of airway hyperresponsiveness to hypertonic saline.21 Healthy controls without asthma (n = 13) were recruited by advertisement. Exclusion criteria included recent (past month)
Results
Characteristics of the participants are summarized in Table I. The patients with asthma (n = 59) had a mean age (SD) of 58 (14) years and moderate lung function impairment with a mean FEV1% predicted (SD) of 76 (20). There were 25 males and 34 females, and 40 (68%) participants were atopic. Forty-one (69%) people were taking inhaled corticosteroids with a median (Q1-Q3) daily dose of 1000 (400-2000) μg beclomethasone equivalents/d. Twenty-eight (47%) of participants were exsmokers, with a
Discussion
This study demonstrates the use of unsupervised hierarchical clustering of induced sputum gene expression profiles to identify 3 TAPs occurring in the studied population. These 3 distinct phenotypes relate to both the clinical asthma status and the type and degree of airway inflammation present, providing further validation for their existence and relevance. The first 2 TAPs are inflammation-predominant, with TAP1 eosinophil-enriched and TAP2 neutrophil-enriched. The eosinophil-enriched group
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Supported by the John Hunter Hospital Charitable Trust, HMRI, and XStrata Coal.
Disclosure of potential conflict of interest: P. G. Gibson has received honoraria from GlaxoSmithKline, AstraZeneca, and Novartis. The rest of the authors have declared that they have no conflict of interest.