Background Recent evidence suggests that burn patients are at increased risk of hospital admission for infection, mental health conditions, cardiovascular disease and cancer for many years after discharge for the burn injury itself. Burn injury has also been shown to induce sustained immune system dysfunction. This change to immune function may contribute to the increased risk of chronic disease observed. However, the mechanisms that disrupt long-term immune function in response to burn trauma, and their link to long-term morbidity, remain unknown. In this study we investigated changes to immune function after burn injury using a murine model of non-severe injury. Methods An established mouse model of non-severe burn injury (full thickness burn equivalent to 8% total body surface area) was used in combination with an orthotopic model of B16 melanoma to investigate the link between burns and cancer. Considering that CD8+ T cells are important drivers of effective tumour suppression in this model, we also investigated potential dysregulation of this immune population using mouse models of burn injury in combination with herpes simplex virus infection. Flow cytometry was used to detect and quantify cell populations of interest and changes in immune function. Results We demonstrate that 4 weeks after a non-severe burn injury, mice were significantly more susceptible to tumour development than controls using an orthotopic model of B16 melanoma. In addition, our results reveal that CD8+ T cell expansion, differentiation and memory potential is significantly impaired at 1 month post-burn. Conclusions Our data suggests that CD8+ T cell-mediated immunity may be dysfunctional for a sustained period after even non-severe burn injury. Further studies in patients to validate these findings may support clinical intervention to restore or protect immunity in patients after burn injury and reduce the increased risk of secondary morbidities observed.

中文翻译：

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非严重烧伤会增加小鼠的癌症发病率，并对 T 细胞的激活和功能产生长期影响。

背景 最近的证据表明，烧伤患者在因烧伤本身出院多年后，因感染、心理健康状况、心血管疾病和癌症入院的风险增加。烧伤也被证明会导致持续的免疫系统功能障碍。这种免疫功能的变化可能会导致观察到的慢性病风险增加。然而，破坏长期免疫功能以应对烧伤的机制，以及它们与长期发病率的联系，仍然未知。在这项研究中，我们使用非严重损伤的小鼠模型研究了烧伤后免疫功能的变化。方法 建立的非重度烧伤小鼠模型（全层烧伤相当于全身表面积的8%）与B16黑色素瘤原位模型相结合，研究烧伤与癌症之间的联系。考虑到 CD8+ T 细胞是该模型中有效抑制肿瘤的重要驱动因素，我们还使用烧伤小鼠模型结合单纯疱疹病毒感染研究了该免疫群体的潜在失调。流式细胞术用于检测和量化感兴趣的细胞群和免疫功能的变化。结果 我们证明，在非严重烧伤 4 周后，使用 B16 黑色素瘤原位模型的小鼠比对照组更容易发生肿瘤。此外，我们的结果表明，CD8+ T 细胞扩增，烧伤后 1 个月，分化和记忆潜能显着受损。结论 我们的数据表明，即使在非严重烧伤损伤后，CD8+ T 细胞介导的免疫功能也可能在一段持续时间内出现功能障碍。对患者进行进一步研究以验证这些发现可能支持临床干预，以恢复或保护烧伤后患者的免疫力，并降低观察到的继发性疾病风险增加。