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Bronchial Inflammation*: Its Relationship to Colonizing Microbial Load and α1-Antitrypsin Deficiency

Robert A. Stockley, DSc, MD; Adam T. Hill, MB ChB; Susan L. Hill, PhD; Edward J. Campbell, MD
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*From the Department of Medicine (Drs. Stockley, Hill, and Hill), Queen Elizabeth Hospital, Birmingham B15 2TH, UK; and the University of Utah (Dr. Campbell), Salt Lake City, UT.

Correspondence to: Robert A. Stockley, DSc, MD, Department of Medicine, Queen Elizabeth Hospital, Birmingham B15 2TH, UK



Chest. 2000;117(5_suppl_1):291S-293S. doi:10.1378/chest.117.5_suppl_1.291S
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Neutrophil elastase is capable of generating many of the features of chronic bronchial disease. In patients with COPD, airways inflammation with neutrophil recruitment and elastase release is positively correlated with colonizing bacterial load in the stable clinical state (p < 0.0005). In addition, α1-antitrypsin deficiency is associated with a greater neutrophil load, higher elastase activity, leukotriene-B4 concentration, and serum protein leak than matched patients without deficiency (p < 0.005). These data confirm an effect of bronchial colonization on airways inflammation in COPD and indicate the role of α1-antitrypsin in its modulation.

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