Proceedings of the American Thoracic Society Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chua, F.
Right arrow Articles by Laurent, G. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chua, F.
Right arrow Articles by Laurent, G. J.
The Proceedings of the American Thoracic Society 3:424-427 (2006)
© 2006 The American Thoracic Society

Neutrophil Elastase

Mediator of Extracellular Matrix Destruction and Accumulation

Felix Chua and Geoffrey J. Laurent

Centre of Respiratory Research, Royal Free and University College London Medical School, London, United Kingdom

Correspondence and requests for reprints should be addressed to Geoffrey J. Laurent, Ph.D., Centre for Respiratory Research, Royal Free and University College London Medical School, Rayne Building, 5 University Street, London WC1E 6JJ, UK. E-mail: g.laurent{at}ucl.ac.uk

ABSTRACT

Of the myriad proteolytic enzymes implicated in the development of lung disease, neutrophil elastase has undoubtedly some of the most versatile effects. Although its key physiologic role is in innate host defense, it can also participate in tissue remodeling and possesses secretagogue actions that are now recognized as important to local inflammatory responses. Although unopposed neutrophil elastase activity has been implicated in the development of emphysema for several decades, only relatively recently has a pathogenetic function been ascribed to this serine proteinase in situations where excessive extracellular matrix deposition occurs. The use of genetically manipulated animal models is starting to uncover the potential ways in which its actions might influence fibrotic lung repair. Emerging evidence suggests that the engagement of cellular pathways with more direct effects on fibrogenic mediator generation and collagen synthesis appears to underpin the actions of neutrophil elastase in promoting lung matrix accumulation.

Key Words: emphysema • pulmonary fibrosis • transforming growth factor-ß




This article has been cited by other articles:


Home page
 INT J LOW EXTREM WOUNDSHome page
D. R. Yager, R. A. Kulina, and L. A. Gilman
Wound Fluids: A Window Into the Wound Environment?
International Journal of Lower Extremity Wounds, December 1, 2007; 6(4): 262 - 272.
[Abstract] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
A. Churg, H. Tai, T. Coulthard, R. Wang, and J. L. Wright
Cigarette Smoke Drives Small Airway Remodeling by Induction of Growth Factors in the Airway Wall
Am. J. Respir. Crit. Care Med., December 15, 2006; 174(12): 1327 - 1334.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the American Thoracic Society.