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首页> 外文期刊>Wound repair and regeneration: official publication of the Wound Healing Society [and] the European Tissue Repair Society >Delayed wound healing in diabetic (db/db) mice with Pseudomonas aeruginosa biofilm challenge: a model for the study of chronic wounds.
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Delayed wound healing in diabetic (db/db) mice with Pseudomonas aeruginosa biofilm challenge: a model for the study of chronic wounds.

机译:铜绿假单胞菌生物膜挑战的糖尿病(db / db)小鼠的伤口愈合延迟:慢性伤口研究模型。

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摘要

Chronic wounds are a major clinical problem that lead to considerable morbidity and mortality. We hypothesized that an important factor in the failure of chronic wounds to heal was the presence of microbial biofilm resistant to antibiotics and protected from host defenses. A major difficulty in studying chronic wounds is the absence of suitable animal models. The goal of this study was to create a reproducible chronic wound model in diabetic mice by the application of bacterial biofilm. Six-millimeter punch biopsy wounds were created on the dorsal surface of diabetic (db/db) mice, subsequently challenged with Pseudomonas aeruginosa (PAO1) biofilms 2 days postwounding, and covered with semiocclusive dressings for 2 weeks. Most of the control wounds were epithelialized by 28 days postwounding. In contrast, none of biofilm-challenged wounds were closed. Histological analysis showed extensive inflammatory cell infiltration, tissue necrosis, and epidermal hyperplasia adjacent to challenged wounds-all indicators of an inflammatory nonhealing wound. Quantitative cultures and transmission electron microscopy demonstrated that the majority of bacteria were in the scab above the wound bed rather than in the wound tissue. The model was reproducible, allowed localized cutaneous wound infections without high mortality, and demonstrated delayed wound healing following a biofilm challenge. This model may provide an approach to study the role of microbial biofilms in chronic wounds as well as the effect of specific biofilm therapy on wound healing.
机译:慢性伤口是导致大量发病和死亡的主要临床问题。我们假设慢性伤口无法治愈的重要因素是存在对抗生素具有抗药性且不受宿主防御的微生物膜的存在。研究慢性伤口的主要困难是缺乏合适的动物模型。这项研究的目的是通过应用细菌生物膜在糖尿病小鼠中创建可重现的慢性伤口模型。在糖尿病(db / db)小鼠的背侧表面创制了6毫米的穿孔活检伤口,随后在伤后2天用铜绿假单胞菌(PAO1)生物膜攻击,并用半封闭敷料覆盖2周。伤口后28天,大多数对照伤口均已上皮。相反,没有生物膜挑战性伤口闭合。组织学分析表明,炎性伤口附近有大量炎性细胞浸润,组织坏死和表皮增生,这是炎性不愈合伤口的所有指标。定量培养和透射电子显微镜显示,大多数细菌在伤口床上方的the中,而不是在伤口组织中。该模型是可重现的,允许局部皮肤伤口感染而无高死亡率,并证明了生物膜刺激后伤口愈合延迟。该模型可以提供一种方法来研究微生物生物膜在慢性伤口中的作用以及特定生物膜疗法对伤口愈合的影响。

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