Department of Dental and Craniofacial Trauma Research, United States Army Institute of Surgical Research, JBSA Fort Sam Houston, San Antonio, TX, United States.
Research Support Division, United States Army Institute of Surgical Research, JBSA Fort Sam Houston, San Antonio, TX, United States.
Front Cell Infect Microbiol. 2020 Jan 10;9:466. doi: 10.3389/fcimb.2019.00466. eCollection 2019.
Burn wound injury affects soldiers and civilians alike, often resulting in a dynamic, but un-orchestrated, host response that can lead to infection, scarring, and potentially death. To mitigate these factors, it is important to have a clinically relevant model of burn wound infection that can be utilized for advancing burn wound treatments. Our previous reports have demonstrated the ability of to generate a biofilm infection within a modified Walker-Mason rat burn model of deep-partial (DPT) and full-thickness (FT) burn wounds (10% total body surface area) in male Sprague-Dawley rats (350-450 g). Here, we further define this model with respect to the host response when challenged with infection between the two burn types. Following burn injury and immediate surface exposure to , inflammation at the local and systemic levels were monitored for an 11 days period. Compared to burn-only groups, infection with further promoted local inflammation in both DPT and FT burn wounds, which was evident by enhanced cellular influx (including neutrophils and monocytes), increased levels of several pro-inflammatory cytokines (IL-1β, IL-6, GRO/KC, andMIP-1α), and reduced IL-10. Systemically, only minor changes were seen in circulating white blood cells and cytokines; however, increases in high mobility group box-1 (HMGB-1) and hyaluronan, as well as decreases in fibronectin were noted particularly in FT burns. Compared to the burn-only group, infection resulted in sustained and/or higher levels of HMGB-1 and hyaluronan. Combined with our previous work that defined the burn depth and development of biofilms within the wound, this study further establishes this model by defining the host response to the burn and biofilm-infection. Furthermore, this characterization shows several similarities to what is clinically seen and establishes this model for future use in the development and testing of novel therapeutics for burn wound treatment at home and on the battlefield.
烧伤伤口损伤影响士兵和平民,通常会导致动态但不协调的宿主反应,从而导致感染、疤痕和潜在的死亡。为了减轻这些因素的影响,重要的是要有一个临床相关的烧伤伤口感染模型,可用于推进烧伤伤口治疗。我们之前的报告已经证明了 在改良的 Walker-Mason 大鼠深部分(DPT)和全层(FT)烧伤模型(10%总体表面积)中产生生物膜感染的能力,该模型在雄性 Sprague-Dawley 大鼠(350-450 g)中使用。在这里,我们进一步定义了这种模型,即在两种烧伤类型下受到 感染时的宿主反应。在烧伤损伤和立即暴露于 后,监测局部和全身炎症反应 11 天。与仅烧伤组相比,感染 进一步促进了 DPT 和 FT 烧伤伤口的局部炎症,这表现为细胞浸润增加(包括中性粒细胞和单核细胞)、几种促炎细胞因子(IL-1β、IL-6、GRO/KC 和 MIP-1α)水平升高和 IL-10 减少。全身性方面,仅观察到循环白细胞和细胞因子的微小变化;然而,HMGB-1 和透明质酸的增加以及纤维连接蛋白的减少在 FT 烧伤中尤为明显。与仅烧伤组相比, 感染导致 HMGB-1 和透明质酸持续和/或更高水平。结合我们之前定义伤口内烧伤深度和 生物膜形成的工作,本研究通过定义宿主对烧伤和生物膜感染的反应进一步建立了该模型。此外,这种特征与临床上所见的情况有几个相似之处,并为今后在家中和战场上开发和测试新型烧伤伤口治疗的治疗方法建立了该模型。