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 Rennard, S. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rennard, S. I.
The Proceedings of the American Thoracic Society 1:282-287 (2004)
© 2004 The American Thoracic Society

Antiinflammatory Therapies Other Than Corticosteroids

Stephen I. Rennard

University of Nebraska Medical Center, Omaha, Nebraska

Correspondence and requests for reprints should be addressed to Stephen I. Rennard, M.D., University of Nebraska Medical Center, 985125 Nebraska Medical Center, Omaha, NE 68198. E-mail: srennard{at}unmc.edu

Antiinflammatory therapy for chronic obstructive pulmonary disease (COPD) can be directed at several stages of the inflammatory process. Much attention has been focused on blocking the damaging effects of toxic mediators released by inflammatory cells, including antioxidants and antiproteases. An alternate strategy is to block the recruitment of inflammatory cells into the lung, such as by inhibiting the production of chemotactic factors driving inflammatory cell recruitment, the ability of inflammatory cells to respond to chemotactic factors, and the ability of inflammatory cells to migrate. Moreover, mediators released by inflammatory cells, particularly tumor necrosis factor-{alpha}, probably have systemic effects in COPD. Blocking the release of these cytokines or blocking their ability to act on distal tissues represents another potential therapeutic option. It is also important to recognize that the various components of the inflammatory response are not independent. The action of proteases released by inflammatory cells, for example, can generate chemotactic factors, lead to activation of inflammatory cells, and modulate repair responses. The complex network of regulatory molecules that controls the inflammatory response, therefore, presents a number of potential therapeutic targets with the promise of altering the disease process in COPD.

Key Words: antiproteases • lung repair • oxidants • proteases • tumor necrosis factor-{alpha}




This article has been cited by other articles:


Home page
ERRHome page
S. I. Rennard
Inflammation in COPD: a link to systemic comorbidities
Eur. Respir. Rev., September 1, 2007; 16(105): 91 - 97.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
A. A. Elmarakby, J. E. Quigley, D. M. Pollock, and J. D. Imig
Tumor Necrosis Factor {alpha} Blockade Increases Renal Cyp2c23 Expression and Slows the Progression of Renal Damage in Salt-Sensitive Hypertension
Hypertension, March 1, 2006; 47(3): 557 - 562.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2004 by the American Thoracic Society.