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(American Journal of Pathology. 2007;170:188-202.)
© 2007 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2007.060370

Accelerated Wound Closure in Mice Deficient for Interleukin-10

Sabine A. Eming^*, Sabine Werner, Philippe Bugnon, Claudia Wickenhauser, Lisa Siewe^*, Olaf Utermöhlen, Jeffrey M. Davidson^¶||, Thomas Krieg^* and Axel Roers^*

From the Department of Dermatology^* and the Institutes for Pathology and Medical Microbiology, Immunology, and Hygiene, University of Cologne, Cologne, Germany; the Department of Biology, Institute of Cell Biology, Eidgenössische Technische Hochschule Zurich, Honggerberg, Switzerland; the Department of Pathology,^¶ Vanderbilt University School of Medicine, Nashville, Tennessee; and the Research and Development Service Veterans Affairs Tennessee Valley Healthcare System,|| Nashville, Tennessee

The impact of the local inflammatory response on the process of wound healing has been debated for decades. In particular, the question whether infiltrating macrophages and granulocytes promote or impede tissue repair has received much attention. In the present study, we show that wound healing is accelerated in mice deficient for the anti-inflammatory cytokine interleukin (IL)-10. IL-10^–/– mice closed excisional wounds significantly earlier compared with IL-10-competent control littermates. This effect was attributable to accelerated epithelialization as well as enhanced contraction of the wound tissue in the mutant animals. Increased -smooth muscle actin expression in IL-10-deficient mice suggests that augmented myofibroblast differentiation is responsible for the enhanced contraction of wounds in mutant mice. The number of macrophages infiltrating the wound tissue was significantly increased in IL-10^–/– mice compared with control littermates suggesting that this cell type mediates the accelerated tissue repair. These results show for the first time that IL-10 can impede wound repair.

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