Gelfand J A, Donelan M, Hawiger A, Burke J F
J Clin Invest. 1982 Dec;70(6):1170-6. doi: 10.1172/jci110715.
We have studied the role of the complement system in burn injury in an experimental model in mice. A 25% body surface area, full-thickness scald wound was produced in anesthetized animals. Massive activation of the alternative complement pathway, but not the classical pathway, was seen. This activation was associated with the generation of neutrophil aggregating activity in the plasma, neutrophil aggregates in the lungs, increased pulmonary vascular permeability, and increased lung edema formation. Decomplementation with cobra venom factor (CVF) or genetic C5 deficiency diminished these pathologic changes, and CVF pretreatment substantially reduced burn mortality in the first 24 h. Preliminary data show that human burn patients have a similar pattern of complement activation involving predominantly the alternative pathway, indicating the possible relevance of the murine model to human disease.
我们在小鼠实验模型中研究了补体系统在烧伤中的作用。在麻醉动物身上造成了25%体表面积的全层烫伤创面。观察到替代补体途径大量激活，但经典途径未激活。这种激活与血浆中中性粒细胞聚集活性的产生、肺内中性粒细胞聚集、肺血管通透性增加以及肺水肿形成增加有关。用眼镜蛇毒因子（CVF）去补体或遗传性C5缺乏可减轻这些病理变化，并且CVF预处理可显著降低最初24小时内的烧伤死亡率。初步数据表明，人类烧伤患者具有类似的补体激活模式，主要涉及替代途径，这表明小鼠模型与人类疾病可能具有相关性。
