Chest ACCP Education Calendar
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Stockley, R. A.
Right arrow Articles by Campbell, E. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Stockley, R. A.
Right arrow Articles by Campbell, E. J.
(Chest. 2000;117:291S-293S.)
© 2000 American College of Chest Physicians

Bronchial Inflammation*

Its Relationship to Colonizing Microbial Load and {alpha}1-Antitrypsin Deficiency

Robert A. Stockley, DSc, MD; Adam T. Hill, MB ChB; Susan L. Hill, PhD and Edward J. Campbell, MD

* 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

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, {alpha}1-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 {alpha}1-antitrypsin in its modulation.

Key Words: {alpha}1-antitrypsin deficiency • bacteria • COPD • inflammation






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2000 by the American College of Chest Physicians.