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* From the National Jewish Medical and Research Center, University of Colorado Health Sciences Center, Denver, CO.
Correspondence to: Philip E. Silkoff, MD, FCCP, National Jewish Medical and Research Center, 1400 Jackson St, Denver, CO 80206; e-mail: silkoffp{at}njc.org
Airway inflammation in severe asthma may indicate prognosis and guide therapy. Noninvasive assessment of airway inflammation using induced sputum (IS) could allow monitoring of response to therapy. The late fraction of IS has been reported to sample the distal lung more than the early fraction.1 We examined whether early IS collection (E-IS; first 10 min) and late IS collection (L-IS; second 10 min) of differentials correlated with BAL and endobronchial biopsy inflammatory cells in normal subjects, and subjects with mild, moderate, and severe asthma.
E-IS showed a significantly raised neutrophil count compared to L-IS (n = 18, p = 0.02) but no difference in total cell count; all other cell types, including epithelial and squamous cells, were not significantly different between the two collections. E-IS and BAL eosinophils were significantly correlated (n = 20,
= 0.72, p = 0.0004) in all groups and in asthma alone (n = 10,
= 0.82, p = 0.004); L-IS showed weaker correlations for percentage of eosinophils with BAL (
= 0.51, p = 0.05 in all groups;
= 0.81, p = 0.049 in asthma). There were no significant correlations between either E-IS or L-IS with BAL for other cell types, and no significant correlations of E-IS or L-IS inflammatory cells with any submucosal cell types (lymphocytes-CD3, macrophages-CD68, neutrophil, or activated eosinophils-EG2+).
E-IS and to a lesser extent L-IS were highly correlated with BAL for eosinophils in all groups and in asthma, but did not correlate with endobronchial biopsy submucosal inflammatory cell counts. This may be attributed to the fact that sputum and BAL sample the airway lumen, whereas the cellular inflammation in the airway submucosa may be distinct. IS could be used to monitor luminal eosinophilic inflammation but probably not mucosal inflammation in asthma.
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Funded by HL-64087, AI-40600, American Lung Association of Colorado, and RR00015.
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