Diabetes
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 Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Goren, I.
Right arrow Articles by Frank, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Goren, I.
Right arrow Articles by Frank, S.
Social Bookmarking
Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes 52:2821-2832, 2003
© 2003 by the American Diabetes Association, Inc.

Leptin and Wound Inflammation in Diabetic ob/ob Mice

Differential Regulation of Neutrophil and Macrophage Influx and a Potential Role for the Scab as a Sink for Inflammatory Cells and Mediators

Itamar Goren1, Heiko Kämpfer1, Maurizio Podda2, Josef Pfeilschifter1, and Stefan Frank1

1 Pharmazentrum Frankfurt, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany
2 Zentrum der Dermatologie und Venerologie, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany

In this study, we investigated the role of leptin for the inflammatory response in diabetes-impaired skin repair. We demonstrated, that systemic treatment of diabetic ob/ob mice with leptin blunted polymorphonuclear neutrophil (PMN), but not macrophage influx into the wound site. Closed wounds of leptin-administered mice were characterized by tremendous numbers of macrophage within the granulation tissue. In line, leptin supplementation potently attenuated epithelium-derived CXC- but not CC-chemokine expression. PMNs were preferentially located in the scab, but macrophages predominantly resided within the wound stroma of the animals. The scabs of nonhealing wounds were most likely to serve as sinks for bioactive inflammatory mediators, which were still capable to drive gene expression in keratinocytes in vitro. Differential effects of leptin on PMN and macrophage axes of inflammation must be indirect, as topical administration of leptin onto wounds of ob/ob mice did not reduce PMN influx into the wounded areas. Moreover, caloric-restricted, pair-fed ob/ob mice were characterized by impaired healing conditions that were associated with persisting PMNs. Interestingly, we documented the absence of leptin receptor expression in human diabetic foot ulcers. Thus, we show that leptin might function as a regulatory link between the endocrine and the immune system in the context of skin repair.

Address correspondence and reprint requests to Dr. Stefan Frank, Pharmazentrum Frankfurt, Institut für Allgemeine Pharmakologie und Toxikologie Klinikum der JW Goethe-Universität Frankfurt/M., Theodor-Stern-Kai 7, D-60590 Frankfurt/M., Germany. E-mail: s.frank{at}em.uni-frankfurt.de


Add to CiteULike CiteULike   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 Mol. Pharmacol.Home page
D. Schiefelbein, O. Seitz, I. Goren, J. P. Dissmann, H. Schmidt, M. Bachmann, R. Sader, G. Geisslinger, J. Pfeilschifter, and S. Frank
Keratinocyte-Derived Vascular Endothelial Growth Factor Biosynthesis Represents a Pleiotropic Side Effect of Peroxisome Proliferator-Activated Receptor-{gamma} Agonist Troglitazone but Not Rosiglitazone and Involves Activation of p38 Mitogen-Activated Protein Kinase: Implications for Diabetes-Impaired Skin Repair
Mol. Pharmacol., October 1, 2008; 74(4): 952 - 963.
[Abstract] [Full Text] [PDF]

Home page
 Rheumatology (Oxford)Home page
P. Kumpers, R. Horn, G. Brabant, A. Woywodt, M. Schiffer, H. Haller, and M. Haubitz
Serum leptin and ghrelin correlate with disease activity in ANCA-associated vasculitis
Rheumatology, April 1, 2008; 47(4): 484 - 487.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
L. Macia, M. Delacre, G. Abboud, T.-S. Ouk, A. Delanoye, C. Verwaerde, P. Saule, and I. Wolowczuk
Impairment of Dendritic Cell Functionality and Steady-State Number in Obese Mice
J. Immunol., November 1, 2006; 177(9): 5997 - 6006.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
I. Goren, E. Muller, J. Pfeilschifter, and S. Frank
Severely Impaired Insulin Signaling in Chronic Wounds of Diabetic ob/ob Mice: A Potential Role of Tumor Necrosis Factor-{alpha}
Am. J. Pathol., March 1, 2006; 168(3): 765 - 777.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
G. Sosne, P. L. Christopherson, R. P. Barrett, and R. Fridman
Thymosin-{beta}4 Modulates Corneal Matrix Metalloproteinase Levels and Polymorphonuclear Cell Infiltration after Alkali Injury
Invest. Ophthalmol. Vis. Sci., July 1, 2005; 46(7): 2388 - 2395.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
A. Bruno, S. Conus, I. Schmid, and H.-U. Simon
Apoptotic Pathways Are Inhibited by Leptin Receptor Activation in Neutrophils
J. Immunol., June 15, 2005; 174(12): 8090 - 8096.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
H. Kampfer, R. Schmidt, G. Geisslinger, J. Pfeilschifter, and S. Frank
Wound Inflammation in Diabetic ob/ob Mice: Functional Coupling of Prostaglandin Biosynthesis to Cyclooxygenase-1 Activity in Diabetes-Impaired Wound Healing
Diabetes, May 1, 2005; 54(5): 1543 - 1551.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 2003 by the American Diabetes Association.