Exacerbated and prolonged inflammation impairs wound healing and increases scarring
Exacerbated and prolonged inflammation impairs wound healing and increases scarring
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DOI：
10.1111/wrr.12381
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发表时间：
2016-01-01
影响因子：
2.9
通讯作者：
Leung, Kai P.
中科院分区：
文献类型：
--
作者：
Qian, Li-Wu;Fourcaudot, Andrea B.;Leung, Kai P.
长期以来，早期炎症的改变被认为会影响修复过程的后续步骤，从而可能影响正确的伤口愈合和重塑。然而，缺乏明确的实验数据使得伤口炎症调节失调和伤口愈合不良之间的联系难以捉摸。为了弥补这一差距，我们使用已建立的兔耳增生性瘢痕模型来研究失调炎症的原因。我们通过结合创伤相关刺激物、来自热致死的铜绿假单胞菌的病原体相关分子模式和来自真皮匀浆的损伤相关分子模式，在这些伤口中诱导了一种加重和持续的炎症状态。在模拟创面中，根据对IL-6表达、组织多形核白细胞浸润和组织髓过氧化物酶活性的定量测量，观察到炎症的加剧和延长。与非刺激对照组相比，在术后第7天和第16天，与非刺激对照组相比，刺激创面的伤口愈合参数(上皮细胞间隙和其他)发生了显著变化。术后第35天，刺激创面瘢痕升高指数为1.90，高于对照创面(P<0.05)。
Altered inflammation in the early stage has long been assumed to affect subsequent steps of the repair process that could influence proper wound healing and remodeling. However, the lack of explicit experimental data makes the connection between dysregulated wound inflammation and poor wound healing elusive. To bridge this gap, we used the established rabbit ear hypertrophic scar model for studying the causal effect of dysregulated inflammation. We induced an exacerbated and prolonged inflammatory state in these wounds with the combination of trauma-related stimulators of pathogen-associated molecular patterns from heat-killed Pseudomonas aeruginosa and damage-associated molecular patterns from a dermal homogenate. In stimulated wounds, a heightened and lengthened inflammation was observed based on quantitative measurements of IL-6 expression, tissue polymorphonuclear leukocytes infiltration, and tissue myeloperoxidase activity. Along with the high level of inflammation, wound healing parameters (epithelial gap and others) at postoperative day 7 and 16 were significantly altered in stimulated wounds compared to unstimulated controls. By postoperative day 35, scar elevation of stimulated wounds was higher than that of control wounds (scar elevation index: 1.90 vs. 1.39, p