Abstract

Simple SummaryPatients with severe burn injuries undergo surgical procedures to remove dead skin and underlying tissue. The study of tissue damage inflicted by burns is vital for further improving current treatments. Numerous animal burn models have been employed to inflict burns at different temperatures and study the local reaction of harmed tissue and its consequences for the whole organism. Because human skin tissue is different than that of animals, we used human skin tissue discarded from surgeries and exposed the tissue to different burn injuries. The samples were maintained for seven days to study the course of burn damage and activation of different cells in human skin tissue. Our study shows that milder burns result in slowly expanding damage, while severe burns cause deep persistent damage to the skin and underlying fat tissue. These different patterns were also reflected by the activation of immune and repair cells within the fat tissue. Our study suggests that fat tissue adjacent to burn wounds can play a crucial role in tissue repair. Thus, examination of fat tissue vitality before surgery may improve outcomes.Comparative studies of human tissue damage caused by burns are challenging because precise information regarding the temperature, time, and duration of the exposure is often missing. Animal models cannot be fully translated to the human system due to interspecies differences in cutaneous tissues. We used a human composite tissue model to compare tissue damage caused by thermal burns with different dynamics. Equal subcutaneous/cutaneous composite tissue samples from six donors were first exposed to either preheated steel (100 °C) or a precision flame burner (300 °C) and were then maintained in vitro for seven days. Histological and immunohistochemical analyses revealed that flame burns instantly caused deep and stable damage to the subcutaneous tissue, which stayed constant for seven days. By contrast, contact burns inflicted tissue damage that was initially superficial but then expanded deeper into the adipose tissue. This spatiotemporal expansion of tissue damage was essentially accompanied by macrophage and fibroblast activation, which points towards inflammation resolution and wound healing. Our study suggests that thermal differences in burns directly influence the course of tissue damage, the cellular response and, consequently, the likely dynamics of repair processes days after burn injuries.

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