Pattern of airway inflammation and its determinants in children with acutesevere asthma

The aim of this study was to examine the relationship between sputum cell c ounts and clinical variables in children with an acute exacerbation of asth ma. Sputum was successfully obtained from 37 of 42 children presenting to t he Emergency Department with acute asthma, using ultrasonically nebulized n ormal saline (n = 19) or spontaneous expectoration (n = 18). Sputum portion s 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 = 1 6 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 i n 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 exacerbatio n was not related to the inflammatory cell profile. Logistic regression ide ntified maintenance asthma treatment (odds ratio (OR), 5.9; 95% confidence interval (Cl), 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 a sthma preventer therapy (P = 0.001). In conclusion, we identified three distinct patterns of airway inflammation in children with acute asthma; they included increased eosinophils, combin ed eosinophilic-neutrophilic infiltration, and a noneosinophilic pattern. E osinophil degranulation was greatest with the combined eosinophilic/neutrop hilic pattern of airway inflammation. Sputum eosinophils were associated wi th 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 trea tment strategies. (C) 1999 Wiley-Liss, Inc.