Inflammation in wound repair: molecular and cellular mechanisms.
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.
Eming
Sabine A
SA
Department of Dermatology, University of Cologne, Cologne, Germany. sabine.eming@uni-koeln.de
Krieg
Thomas
T
Davidson
Jeffrey M
JM
D000818:Animals; D002478:Cells, Cultured; D005347:Fibroblasts / Q000378:metabolism; D006801:Humans; D007249:Inflammation; D015603:Keratinocytes / Q000378:metabolism; D051379:Mice; D008954:Models, Biological; D009369:Neoplasms / Q000378:metabolism; D010641:Phenotype; D012867:Skin / Q000276:immunology / Q000473:pathology; D014945:Wound Healing