The acute systemic inflammatory response syndrome (SIRS) and multiorgan dysfunction (MOD) that occur in large burn injuries may be attributed, in part, to immunosuppressive responses such as decreased lymphocytes. However, the mitochondrial bioenergetics of lymphocytes after severe burn injury are poorly understood. The purpose of this study was to examine mitochondrial function of lymphocytes following severe burns in a swine model. Anesthetized Yorkshire swine (n = 17) sustained 40% total body surface area full-thickness contact burns. Blood was collected at pre-injury (Baseline; BL) and at 24 and 48 h after injury for complete blood cell analysis, flow cytometry, cytokine analysis, and ficoll separation of intact lymphocytes for high-resolution mitochondrial respirometry analysis. While neutrophil numbers increased, a concomitant decrease was found in lymphocytes (P < 0.001) after burn injury, which was not specific to CD4⁺ or CD8⁺ lymphocytes. No changes in immune cell population were observed from 24 h to 48 h post-injury. IL 12-23 decreased while a transient increase in IL 4 was found from BL to 24h (P < 0.05). CRP progressively increased from BL to 24h (P < 0.05) and 48h (P < 0.001) post-injury. Routine and maximal mitochondrial respiration progressively increased from BL to 24h (P < 0.05) and 48 h post-injury (P < 0.001). No changes were found in leak respiration or residual oxygen consumption. When considering the reduction in lymphocyte number, the total peripheral lymphocyte bioenergetics per volume of blood significantly decreased from BL to 24h and 48h (P < 0.05). For the first time, we were able to measure mitochondrial activity in intact lymphocyte mitochondria through high-resolution respirometry in a severely burned swine model. Our data showed that the non-specific reduction in peripheral T cells after injury was larger than the increased mitochondrial activity in those cells, which may be a compensatory mechanism for the total reduction in lymphocytes. Additional studies in the metabolic activation of T cell subpopulations may provide diagnostic or therapeutic targets after severe burn injury.

严重烧伤中发生的急性全身炎症反应综合征（SIRS）和多器官功能障碍（MOD）可能部分归因于免疫抑制反应，例如淋巴细胞减少。但是，严重烧伤后淋巴细胞的线粒体生物能学知之甚少。这项研究的目的是检查猪模型严重烧伤后淋巴细胞的线粒体功能。麻醉的约克郡猪（n = 17）持续40％的全身表面积全层接触灼伤。在受伤前（基线； BL）以及受伤后24和48 h收集血液，以进行完整的血细胞分析，流式细胞术，细胞因子分析和完整淋巴细胞的ficoll分离，以进行高分辨率的线粒体呼吸测定法分析。虽然中性粒细胞数量增加，但 烧伤后淋巴细胞却伴有减少（P <0.001），这对CD4 ⁺或CD8 ⁺淋巴细胞不是特异性的。从损伤后24小时至48小时未观察到免疫细胞群的变化。IL 12-23降低，而从BL到24h IL 4瞬时升高（P  <0.05）。CRP从BL逐渐增加到24h（P 受伤后 <0.05）和48小时（P <0.001）。常规和最大线粒体呼吸从BL逐渐增加到 受伤后24h（P <0.05）和损伤后48 h（P <0.001）。泄漏呼吸或残余氧气消耗均未发现变化。当考虑减少淋巴细胞数量时，每单位血液总外周淋巴细胞生物能从BL显着降低至24h和48h（P <0.05）。我们首次能够通过高分辨率呼​​吸测定法在严重烧伤的猪模型中测量完整淋巴细胞线粒体中的线粒体活性。我们的数据表明，损伤后外周T细胞的非特异性减少大于这些细胞中线粒体活性的增加，这可能是淋巴细胞总数减少的一种补偿机制。T细胞亚群代谢活化的其他研究可提供严重烧伤后的诊断或治疗靶标。