Abstract
Every year, thousands of soldiers and civilians succumb to burn wound trauma with highly unfavorable outcomes. We previously established a modified Walker-Mason rat scald model exhibiting a P. aeruginosa infection. Here we characterize deep partial- (DPT) and full-thickness (FT) burn wounds inoculated with Staphylococcus aureus. Male Sprague-Dawley rats (350–450 g) inflicted with 10% total body surface area burn inoculated with S. aureus (103–5 CFU/wound) were monitored over an 11-day period. S. aureus rapidly dominated the wound bed, with bacterial loads reaching at least 1 × 109 CFU/g tissue in all wounds. Within 3 days, S. aureus biofilm formation occurred based on genetic transcripts and Giemsa staining of the tissue. S. aureus infection resulted in a slightly faster recruitment of neutrophils in FT wounds, which was related to necrotic neutrophils. The extent of the inflammatory response in S. aureus infected burn wounds correlated with elevated G-CSF, GM-CSF, GRO/KC and/or TNF-α levels, but a majority of pro- and anti-inflammatory cytokines (IL-1β, IL-6, IFN-γ, IL-10, and IL-13) were found to be suppressed, compared to burn-only controls. S. aureus infection resulted in dynamic changes in DAMPs, including elevated HMGB-1 and reduced levels of circulating hyaluronan within FT wounds. S. aureus also reduced complement C3 at all time points in DPT and FT wounds. These changes in DAMPs are believed to be correlated with burn severity and S. aureus specific bioburden. Collectively, this model showcases the evasiveness of S. aureus through dampening the immune response to flourish in the burn wound.
Highlights
Burn injury is a traumatic event that breaches the barrier between the human’s environment and the first line of defense—the skin
The total bioburden within the FT burn-only controls increased more steadily and consistently compared to deep partial- (DPT) burn-only; the DPT controls had a slightly elevated bioburden by post-operative day (POD) 11 (Figure 1B)
S. aureus exposure following DPT and FT burn injury resulted in rapid biofilm formation within the wound bed
Summary
Burn injury is a traumatic event that breaches the barrier between the human’s environment and the first line of defense—the skin. Similar trends of TBSA and burn location have been noted within the civilian world [8], where there are an estimated 180,000 deaths per year worldwide caused by fire [9]. Of those hospitalized, studies have identified infection as the root cause of death for 42–65% of burn patients, which again stems from the immune-compromised state of the victim [10,11,12,13]. This speaks to the need for clear models of burn wounds that recapitulate the infective scenario, i.e., infections and diverse host responses elicited, and provide avenues for testing novel therapeutics
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