Pattern of airway inflammation and its determinants in children with acute severe asthma.
The aim of this study was to examine the relationship between sputum cell counts and clinical variables in children with an acute exacerbation of asthma. Sputum was successfully obtained from 37 of 42 children presenting to the Emergency Department with acute asthma, using ultrasonically nebulized normal saline (n = 19) or spontaneous expectoration (n = 18). Sputum portions were selected and dispersed, and total and differential cell counts were performed. Sputum supernatant was assessed for eosinophil cationic protein (ECP), interleukin (IL)-5, and IL-8. The exacerbations were of 3 inflammatory cell patterns: eosinophilic (n = 16 or 43% of total), combined eosinophilic/neutrophilic (E/N; n = 13.3 or 35% of total), or noneosinophilic (n = 8 or 22% of total). IL-5 was highest in eosinophilic exacerbations. Combined E/N exacerbations had increased mast cells (77%) and higher sputum ECP levels than eosinophilic exacerbations: 2,146 ng/mL vs. 666 ng/mL (P = 0.04). The speed of onset of the exacerbation was not related to the inflammatory cell profile. Logistic regression identified maintenance asthma treatment (odds ratio (OR), 5.9; 95% confidence interval (CI), 1.3-26.8) and lung function during the acute episode (OR, 4.0; 95% CI, 1.7-93) as significantly associated with the intensity of sputum eosinophilia. Eosinophils were lowest in children who received maintenance treatment with oral corticosteroids compared to those with no background asthma preventer therapy (P = 0.001). In conclusion, we identified three distinct patterns of airway inflammation in children with acute asthma; they included increased eosinophils, combined eosinophilic-neutrophilic infiltration, and a noneosinophilic pattern. Eosinophil degranulation was greatest with the combined eosinophilic/neutrophilic pattern of airway inflammation. Sputum eosinophils were associated with clinical severity, and background asthma therapy, but not with outcome, nor with speed of onset of exacerbations. These different inflammatory cell profiles imply different etiological agents and may require differing treatment strategies.
Gibson
P G
PG
Airway Research Centre, Respiratory Medicine Unit, John Hunter Hospital and School of Paediatrics, University of New South Wales, Randwick, New South Wales, Australia. mdpgg@mail.newcastle.edu.au
Norzila
M Z
MZ
Fakes
K
K
Simpson
J
J
Henry
R L
RL
D000208:Acute Disease; D000293:Adolescent; D001249:Asthma / Q000473:pathology* / Q000503:physiopathology; D016535:Bronchial Hyperreactivity / Q000473:pathology* / Q000503:physiopathology; D001985:Bronchial Provocation Tests; D002648:Child; D016001:Confidence Intervals; D004802:Eosinophilia / Q000473:pathology*; D005260:Female; D006801:Humans; D007958:Leukocyte Count; D016015:Logistic Models; D008297:Male; D009504:Neutrophils / Q000473:pathology; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D013183:Sputum / Q000166:cytology*; D018709:Statistics, Nonparametric