AJP - Lung AJP: Endocrinology and Metabolism
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol 291: L479-L486, 2006. First published March 31, 2006; doi:10.1152/ajplung.00518.2005
1040-0605/06 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
291/3/L479    most recent
00518.2005v1
Right arrow Alert me when this article is cited
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 ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (4)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Boodoo, S.
Right arrow Articles by Horton, M. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Boodoo, S.
Right arrow Articles by Horton, M. R.

Differential regulation of hyaluronan-induced IL-8 and IP-10 in airway epithelial cells

Sada Boodoo,1 Ernst W. Spannhake,2 Jonathan D. Powell,3 and Maureen R. Horton1,2

Departments of 1Medicine and 3Oncology, Johns Hopkins University School of Medicine, and 2Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland

Submitted 9 December 2005 ; accepted in final form 26 March 2006

Airway epithelium is emerging as a regulator of local inflammation and immune responses. However, the cellular and molecular mechanisms responsible for the immune modulation by these cells have yet to be fully elucidated. At the cellular level, the hallmarks of airway inflammation are mucus gland hypertrophy with excess mucus production, accumulation of inflammatory mediators, inflammation in the airway walls and lumen, and breakdown and turnover of the extracellular matrix. We demonstrate that fragments of the extracellular matrix component hyaluronan induce inflammatory chemokine production in primary airway epithelial cells grown at an air-liquid interface. Furthermore, hyaluronan fragments use two distinct molecular pathways to induce IL-8 and IFN-{gamma}-inducible protein 10 (IP-10) chemokine expression in airway epithelial cells. Hyaluronan-induced IL-8 requires the MAP kinase pathway, whereas hyaluronan-induced IP-10 utilizes the NF-{kappa}B pathway. The induction is specific to low-molecular-weight hyaluronan fragments as other glycosaminoglycans do not induce IL-8 and IP-10 in airway epithelial cells. We hypothesize that not only is the extracellular matrix a target of destruction in airway inflammation but it plays a critical role in perpetuating inflammation through the induction of cytokines, chemokines, and modulatory enzymes in epithelial cells. Furthermore, hyaluronan, by inducing IL-8 and IP-10 by distinct pathways, provides a unique target for differential regulation of key inflammatory chemokines.

extracellular matrix; cytokines; interferon {gamma}-inducible protein 10


Address for reprint requests and other correspondence: M. R. Horton, Dept. of Medicine, Div. of Pulmonary and Critical Care Medicine, 1830 E. Monument St., 5th floor, Baltimore, MD 21205 (e-mail: mhorton2{at}jhmi.edu)




This article has been cited by other articles:


Home page
 IOVSHome page
J. Y. Oh, Y. S. In, M. K. Kim, J. H. Ko, H. J. Lee, K. C. Shin, S. M. Lee, W. R. Wee, J. H. Lee, and M. Park
Protective Effect of Uridine on Cornea in a Rabbit Dry Eye Model
Invest. Ophthalmol. Vis. Sci., March 1, 2007; 48(3): 1102 - 1109.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2006 by the American Physiological Society.