Accelerated wound closure in mice deficient for interleukin-10
Accelerated wound closure in mice deficient for interleukin-10
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DOI：
10.2353/ajpath.2007.060370
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发表时间：
2007-01-01
影响因子：
6
通讯作者：
Roers, Axel
中科院分区：
文献类型：
--
作者：
Eming, Sabine A.;Werner, Sabine;Roers, Axel
局部炎症反应对伤口愈合过程的影响已经争论了几十年。尤其是渗透的巨噬细胞和粒细胞是促进还是阻碍组织修复的问题已经引起了人们的广泛关注。在目前的研究中，我们证明了抗炎细胞因子IL-10缺乏的小鼠伤口愈合加快。与IL-10能力强的对照组相比，IL-10(-/-)小鼠闭合切除伤口的时间明显更早。这一效应归因于突变动物伤口组织的上皮化加速和收缩增强。IL-10缺陷小鼠的α-平滑肌肌动蛋白表达增加表明，肌肉成纤维细胞分化增强是突变小鼠伤口收缩增强的原因。M-10(-/-)组小鼠创面组织中巨噬细胞数量较对照组明显增多，提示该细胞类型参与了加速组织修复的过程。这些结果首次表明，IL-10可以阻碍伤口修复。
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 a-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 M-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.