HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 289/5/L842    most recent 00286.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (21) Citing Articles via Google Scholar Google Scholar Articles by Shaykhiev, R. Articles by Bals, R. Search for Related Content PubMed PubMed Citation Articles by Shaykhiev, R. Articles by Bals, R.

Human endogenous antibiotic LL-37 stimulates airway epithelial cell proliferation and wound closure

¹Hospital of the University of Marburg, Department of Internal Medicine, Division of Pulmonary Diseases, Philipps-Universtät Marburg, Marburg; and ²Hospital of the University of Munich, Department of Internal Medicine I, Division of Pulmonary Diseases, Ludwig-Maximilians-Universtät Munich, Munich, Germany

Submitted 26 July 2004 ; accepted in final form 7 June 2005

Antimicrobial peptides are endogenous antibiotics that directly inactivate microorganisms and in addition have a variety of receptor-mediated functions. LL-37/hCAP-18 is the only cathelicidin found in humans and is involved in angiogenesis and regulation of the innate immune system. The aim of the present study was to characterize the role of the peptide LL-37 in the regulation of wound closure of the airway epithelium in the cell line NCI-H292 and primary airway epithelial cells. LL-37 stimulated healing of mechanically induced wounds in monolayers of the cell line and in differentiated primary airway epithelium. This effect was detectable at concentrations of 5 µg/ml in NCI-H292 and 1 µg/ml in primary cells. The effect of LL-37 on wound healing was dependent on the presence of serum. LL-37 induced cell proliferation and migration of NCI-H292 cells. Inhibitor studies in the wound closure and proliferation assays indicated that the effects caused by LL-37 are mediated through epidermal growth factor receptor, a G protein-coupled receptor, and MAP/extracellular regulated kinase. In conclusion, LL-37 induces wound healing, proliferation, and migration of airway epithelial cells. The peptide is likely involved in the regulation of tissue homeostasis in the airways.

airway epithelium; antimicrobial peptide; wound healing; cathelicidin; tissue repair

This article has been cited by other articles:

				R. Bucki, A. G. Sostarecz, F. J. Byfield, P. B. Savage, and P. A. Janmey Resistance of the antibacterial agent ceragenin CSA-13 to inactivation by DNA or F-actin and its activity in cystic fibrosis sputum J. Antimicrob. Chemother., September 1, 2007; 60(3): 535 - 545. [Abstract] [Full Text] [PDF]

				R. Shaykhiev and R. Bals Interactions between epithelial cells and leukocytes in immunity and tissue homeostasis J. Leukoc. Biol., July 1, 2007; 82(1): 1 - 15. [Abstract] [Full Text] [PDF]

				E. Puchelle, J.-M. Zahm, J.-M. Tournier, and C. Coraux Airway Epithelial Repair, Regeneration, and Remodeling after Injury in Chronic Obstructive Pulmonary Disease Proceedings of the ATS, November 1, 2006; 3(8): 726 - 733. [Abstract] [Full Text] [PDF]

				P. G. Barlow, Y. Li, T. S. Wilkinson, D. M. E. Bowdish, Y. E. Lau, C. Cosseau, C. Haslett, A. J. Simpson, R. E. W. Hancock, and D. J. Davidson The human cationic host defense peptide LL-37 mediates contrasting effects on apoptotic pathways in different primary cells of the innate immune system J. Leukoc. Biol., September 1, 2006; 80(3): 509 - 520. [Abstract] [Full Text] [PDF]