Inflammation in wound repair: Molecular and cellular mechanisms

被引:1767
作者
Eming, Sabine A.
Krieg, Thomas
Davidson, Jeffrey M.
机构
[1] Univ Cologne, Dept Dermatol, D-50931 Cologne, Germany
[2] Vanderbilt Univ, Sch Med, Dept Pathol, Nashville, TN 37235 USA
[3] VA Med Ctr, Nashville, TN USA
关键词
D O I
10.1038/sj.jid.5700701
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 [皮肤病与性病学];
摘要
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.
引用
收藏
页码:514 / 525
页数:12
相关论文
共 127 条
[1]
THE POTENTIAL ROLE OF THE LYMPHOCYTE IN FETAL WOUND-HEALING [J].
ADOLPH, VR ;
DISANTO, SK ;
BLEACHER, JC ;
DILLON, PW ;
KRUMMEL, TM .
JOURNAL OF PEDIATRIC SURGERY, 1993, 28 (10) :1316-1320
[2]
Bidirectional regulation of macrophage function by TGF-β [J].
Ashcroft, GS .
MICROBES AND INFECTION, 1999, 1 (15) :1275-1282
[3]
Secretory leukocyte protease inhibitor mediates non-redundant functions necessary for normal wound healing [J].
Ashcroft, GS ;
Lei, KJ ;
Jin, WW ;
Longenecker, G ;
Kulkarni, AB ;
Greenwell-Wild, T ;
Hale-Donze, H ;
McGrady, G ;
Song, XY ;
Wahl, SM .
NATURE MEDICINE, 2000, 6 (10) :1147-1153
[4]
Estrogen modulates cutaneous wound healing by downregulating macrophage migration inhibitory factor [J].
Ashcroft, GS ;
Mills, SJ ;
Lei, KJ ;
Gibbons, L ;
Jeong, MJ ;
Taniguchi, M ;
Burow, M ;
Horan, MA ;
Wahl, SM ;
Nakayama, T .
JOURNAL OF CLINICAL INVESTIGATION, 2003, 111 (09) :1309-1318
[5]
Ageing and wound healing [J].
Ashcroft, GS ;
Mills, SJ ;
Ashworth, JJ .
BIOGERONTOLOGY, 2002, 3 (06) :337-345
[6]
Topical estrogen accelerates cutaneous wound healing in aged humans associated with an altered inflammatory response [J].
Ashcroft, GS ;
Greenwell-Wild, T ;
Horan, MA ;
Wahl, SM ;
Ferguson, MWJ .
AMERICAN JOURNAL OF PATHOLOGY, 1999, 155 (04) :1137-1146
[7]
Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response [J].
Ashcroft, GS ;
Yang, X ;
Glick, AB ;
Weinstein, M ;
Letterio, JJ ;
Mizel, DE ;
Anzano, M ;
Greenwell-Wild, T ;
Wahl, SM ;
Deng, CX ;
Roberts, AB .
NATURE CELL BIOLOGY, 1999, 1 (05) :260-266
[8]
Estrogen accelerates cutaneous wound healing associated with an increase in TGF-beta 1 levels [J].
Ashcroft, GS ;
Dodsworth, J ;
vanBoxtel, E ;
Tarnuzzer, RW ;
Horan, MA ;
Schultz, GS ;
Ferguson, MWJ .
NATURE MEDICINE, 1997, 3 (11) :1209-1215
[9]
Ashcroft GS, 1998, LAB INVEST, V78, P47
[10]
The extracellular adherence protein (Eap) of Staphylococcus aureus inhibits wound heating by interfering with host defense and repair mechanisms [J].
Athanasopoulos, AN ;
Ecnomopoulou, M ;
Orlova, VV ;
Sobke, A ;
Schneider, D ;
Weber, H ;
Augustin, HG ;
Eming, SA ;
Schubert, U ;
Linn, T ;
Nawroth, PP ;
Hussain, MA ;
Hammes, HP ;
Herrmann, M ;
Preissner, KT ;
Chavakis, T .
BLOOD, 2006, 107 (07) :2720-2727