Perspective
Subject Categories: Wound Healing
Journal of Investigative Dermatology (2007) 127, 514–525. doi:10.1038/sj.jid.5700701
Inflammation in Wound Repair: Molecular and Cellular Mechanisms
Editor's Note
Wound healing has been recognized as important to health since the time of Hammurabi. A Sumerian clay tablet (c 2150 BC) described early wound care that included washing the wound in beer and hot water, using poultices from substances such as wine dregs and lizard dung and bandaging the wound. Hippocrates (c 400 BC) detailed the importance of draining pus from the wound, and Galen (c 130–200 AD) described the principle of first and second intention healing (Broughton G et al. (2006) A Brief history of wound care. Plast Reconstr Surg 117:6s). Wound healing advanced slowly over the centuries, with major advances in the 19th century in the importance of controlling infection, hemostasis and necrotic tissue. The discovery of cytokines and growth factors in the 1950s opened a new age in wound healing research and led to many important breakthroughs concerning the basic biology of healing wounds in the skin. In this issue of the JID, a new Perspective series focused on wound healing begins. These articles detail the role of inflammation in wound healing and fibrosis, the key involvement of fibroblasts, myofibroblasts, and keratinocytes in the healing wound, and the great opportunities that tissue engineering provides to improve wound healing. Hippocrates recognized that "Healing is a matter of time, but it is sometimes also a matter of opportunity." These Perspectives show the great new opportunities that we now have for understanding and improving the process of healing wounds of the skin.
Russell P. Hall, III
Deputy Editor
Sabine A Eming1, Thomas Krieg1 and Jeffrey M Davidson2,3
- 1Department of Dermatology, University of Cologne, Cologne, Germany
- 2Department of Pathology, Vanderbilt University School of Medicine, Tennessee, USA
- 3VA Medical Center, Nashville, Tennessee, USA
Correspondence: Dr Sabine A. Eming, Department of Dermatology, University of Cologne, Joseph-Stelzmann Str. 9, 50931 Köln, Germany. E-mail: sabine.eming@uni-koeln.de
Received 30 June 2006; Revised 21 September 2006; Accepted 23 September 2006.
Abstract
In post-natal life the inflammatory response is an inevitable consequence of tissue injury. Experimental studies established the dogma that inflammation is essential to the establishment of cutaneous homeostasis following injury, and in recent years information about specific subsets of inflammatory cell lineages and the cytokine network orchestrating inflammation associated with tissue repair has increased. Recently, this dogma has been challenged, and reports have raised questions on the validity of the essential prerequisite of inflammation for efficient tissue repair. Indeed, in experimental models of repair, inflammation has been shown to delay healing and to result in increased scarring. Furthermore, chronic inflammation, a hallmark of the non-healing wound, predisposes tissue to cancer development. Thus, a more detailed understanding in mechanisms controlling the inflammatory response during repair and how inflammation directs the outcome of the healing process will serve as a significant milestone in the therapy of pathological tissue repair. In this paper, we review cellular and molecular mechanisms controlling inflammation in cutaneous tissue repair and provide a rationale for targeting the inflammatory phase in order to modulate the outcome of the healing response.
Abbreviations:
MCP, monocyte chemoattractant protein-1; MMP, matrix metalloproteinase; PMN, polymorphonuclear leukocyte; ROS, reactive oxygen species; SCC, squamous cell carcinoma; TGF, transforming growth factor; TNF, tumor necrosis factor
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