Organ Support Department, United States (US) Army Institute of Surgical Research, Fort Sam Houston, TX, United States.
Front Immunol. 2023 Jul 14;14:1227751. doi: 10.3389/fimmu.2023.1227751. eCollection 2023.
Acute respiratory distress syndrome (ARDS) is a leading cause of morbidity and mortality in polytrauma patients. Pharmacological treatments of ARDS are lacking, and ARDS patients rely on supportive care. Accurate diagnosis of ARDS is vital for early intervention and improved outcomes but is presently delayed up to days. The use of biomarkers for early identification of ARDS development is a potential solution. Inflammatory mediators high-mobility group box 1 (HMGB1), syndecan-1 (SDC-1), and C3a have been previously proposed as potential biomarkers. For this study, we analyzed these biomarkers in animals undergoing smoke inhalation and 40% total body surface area burns, followed by intensive care for 72 h post-injury (PI) to determine their association with ARDS and mortality. We found that the levels of inflammatory mediators in serum were affected, as well as the degree of HMGB1 and Toll-like receptor 4 (TLR4) signal activation in the lung. The results showed significantly increased HMGB1 expression levels in animals that developed ARDS compared with those that did not. Receiver operating characteristic (ROC) analysis showed that HMGB1 levels at 6 h PI were significantly associated with ARDS development (AUROC=0.77) and mortality (AUROC=0.82). Logistic regression analysis revealed that levels of HMGB1 ≥24.10 ng/ml are associated with a 13-fold higher incidence of ARDS [OR:13.57 (2.76-104.3)], whereas the levels of HMGB1 ≥31.39 ng/ml are associated with a 12-fold increase in mortality [OR: 12.00 (2.36-93.47)]. In addition, we found that mesenchymal stem cell (MSC) therapeutic treatment led to a significant decrease in systemic HMGB1 elevation but failed to block SDC-1 and C3a increases. Immunohistochemistry analyses showed that smoke inhalation and burn injury induced the expression of HMGB1 and TLR4 and stimulated co-localization of HMGB1 and TLR4 in the lung. Interestingly, MSC treatment reduced the presence of HMGB1, TLR4, and the HMGB1-TLR4 co-localization. These results show that serum HMGB1 is a prognostic biomarker for predicting the incidence of ARDS and mortality in swine with smoke inhalation and burn injury. Therapeutically blocking HMGB1 signal activation might be an effective approach for attenuating ARDS development in combat casualties or civilian patients.
急性呼吸窘迫综合征(ARDS)是多发创伤患者发病率和死亡率的主要原因。目前缺乏 ARDS 的药物治疗方法,ARDS 患者只能依靠支持性护理。ARDS 的准确诊断对于早期干预和改善预后至关重要,但目前仍会延迟数天。使用生物标志物来早期识别 ARDS 的发生是一种潜在的解决方案。高迁移率族蛋白 B1(HMGB1)、 syndecan-1(SDC-1)和 C3a 先前被提议作为潜在的生物标志物。在这项研究中,我们分析了经历烟雾吸入和 40%全身表面积烧伤的动物中的这些生物标志物,并在受伤后 72 小时内进行重症监护,以确定它们与 ARDS 和死亡率的关系。我们发现,血清中炎症介质的水平以及肺中 HMGB1 和 Toll 样受体 4(TLR4)信号激活的程度都受到了影响。结果表明,与未发生 ARDS 的动物相比,发生 ARDS 的动物的 HMGB1 表达水平显著升高。受试者工作特征(ROC)分析显示,伤后 6 小时的 HMGB1 水平与 ARDS 的发生(AUROC=0.77)和死亡率(AUROC=0.82)显著相关。Logistic 回归分析显示,HMGB1 水平≥24.10ng/ml 与 ARDS 的发生风险增加 13 倍相关[比值比(OR):13.57(2.76-104.3)],而 HMGB1 水平≥31.39ng/ml 与死亡率增加 12 倍相关[OR:12.00(2.36-93.47)]。此外,我们发现间充质干细胞(MSC)治疗可显著降低全身性 HMGB1 升高,但未能阻断 SDC-1 和 C3a 的升高。免疫组织化学分析表明,烟雾吸入和烧伤损伤诱导了 HMGB1 和 TLR4 的表达,并刺激了 HMGB1 和 TLR4 在肺中的共定位。有趣的是,MSC 治疗减少了 HMGB1、TLR4 和 HMGB1-TLR4 共定位的存在。这些结果表明,血清 HMGB1 是预测烟雾吸入和烧伤伤后猪 ARDS 发生率和死亡率的预后生物标志物。阻断 HMGB1 信号激活可能是减轻战斗伤亡或平民患者 ARDS 发展的有效方法。