Abstract
Many burn interventions aim to target the inflammatory response as a means of enhancing healing or limiting hypertrophic scarring. Murine models of human burns have been developed, but the inflammatory response to injury in these models has not been well defined. The aim of this study was to profile inflammatory cell populations and gene expression relative to healing and scarring in a murine model of thermal burns. Cutaneous injuries were created on the dorsal region of C57Bl/6 mice using a heated metal rod. Animals were euthanized at selected time points over ten weeks, with the lesions evaluated using macroscopic measurements, histology, immunofluorescent histochemistry and quantitative PCR. The burn method generated a reproducible, partial-thickness injury that healed within two weeks through both contraction and re-epithelialization, in a manner similar to human burns. The injury caused an immediate increase in pro-inflammatory cytokine and chemokine expression, coinciding with an influx of neutrophils, and the disappearance of Langerhans cells and mast cells. This preceded an influx of dendritic cells and macrophages, a quarter of which displayed an inflammatory (M1) phenotype, with both populations peaking at closure. As with human burns, the residual scar increased in size, epidermal and dermal thickness, and mast cell numbers over 10 weeks, but abnormal collagen I-collagen III ratios, fibre organization and macrophage populations resolved 3–4 weeks after closure. Characterisation of the inflammatory response in this promising murine burn model will assist future studies of burn complications and aid in the preclinical testing of new anti-inflammatory and anti-scarring therapies.
Highlights
Burns are traumatic injuries that can occur in the home or workplace
To establish the time course of cutaneous healing in mice following a heated metal rod burn, photographs were taken of the healing skin (Figure 1a), with histological analysis conducted on sections of skin biopsies (Figure 1b)
This study demonstrated that a heated metal burn produces a highly reproducible, partial-thickness injury in mice, which mimics key aspects of the inflammatory and hypertrophic scarring responses observed in humans, post burn
Summary
Burns are traumatic injuries that can occur in the home or workplace. There are an estimated 180,000 deaths every year caused by burns, the vast majority in low-middle income countries [1]. While early burn excision and skin grafting has significantly improved outcomes for these patients, slow healing, infections and scarring still provide major challenges to burn care [2]. Thermal and scald burns account for the majority of reported skin burns, with injuries classified as superficial, partial-thickness, full-thickness or subdermal depending on the depth of damage [3]. Partial-thickness burns are classified as superficial or deep, extending to the papillary and reticular dermis, respectively, and can present with blisters, erythema, oedema and diminished sensation. Full-thickness and subdermal burns extend below the skin, and can damage subcutaneous adipose, fascia, muscle or bone. Full-thickness and subdermal burns, are slow to heal, require surgical intervention, lead to hypertrophic scarring, and increase the risk of infection, shock and death. Burn wound extension is clinically important as it can confound diagnosis, treatment selection and patient outcomes
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