Abstract
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 Pseudomonas aeruginosa 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 P. aeruginosa infection between the two burn types. Following burn injury and immediate surface exposure to P. aeruginosa, inflammation at the local and systemic levels were monitored for an 11 days period. Compared to burn-only groups, infection with P. aeruginosa 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, P. aeruginosa 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 P. aeruginosa 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.
Highlights
Burn injury compromises the primary barrier of the host, the skin, which immediately places the host at risk for infection (Church et al, 2006; Kennedy et al, 2010; Lopez et al, 2017)
There was a delayed response in inflammation for FT burns at post-operative days (POD) 1 compared to DPT (Figure 1A)
Research and clinical efforts to understand the effects of burn injury on the host have made it apparent that the response can be highly variable and is governed by several factors related to the injury itself, as well as the patient (Kim et al, 2012)
Summary
Burn injury compromises the primary barrier of the host, the skin, which immediately places the host at risk for infection (Church et al, 2006; Kennedy et al, 2010; Lopez et al, 2017). Research has shown similar trends in both combat and non-combat military situations with regard to burn area and location, which are typically 10% total body surface area (TBSA) and located around the hands and face (Kauvar et al, 2006) These trends were noted to occur in civilian life (Wolf et al, 2006). While hospitalization can be necessary, it may place the patient at a greater risk of infection, formation of biofilms, and even sepsis, leading to greater mortality, especially for patients suffering with greater than a 40% TBSA burn injury (Church et al, 2006; Lopez et al, 2017) These aspects points to the need for continued research efforts in burn therapeutics for both military and civilian application, as well as appropriate pre-clinical models for testing potential therapeutics
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