Cutting edge: HMG-1 as a mediator of acute lung inflammation
Cutting edge: HMG-1 as a mediator of acute lung inflammation
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DOI：
10.4049/jimmunol.165.6.2950
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发表时间：
2000-09-15
影响因子：
4.4
通讯作者：
Tracey, KJ
中科院分区：
文献类型：
--
作者：
Abraham, E;Arcaroli, J;Tracey, KJ
急性炎症性肺损伤是危重病的迟发性并发症，与死亡率增加有关。高迁移率族蛋白1（HMG-1）除了作为转录调节因子外，最近被鉴定为内毒素致死性的晚期介导因子。在本研究中，HMG-I经气管内给药可引起肺急性炎性损伤，伴有中性粒细胞蓄积、肺水肿的发展以及IL-1 β、TNF-α和巨噬细胞炎性蛋白-2的肺产生增加。在内毒素暴露之前或之后施用抗HMG-1 Ab减少了嗜中性粒细胞向肺的迁移以及肺水肿。抗HMG-1的这些保护作用是特异性的，因为在用抗HMG-1治疗后，IL-1 β、TNF-α或巨噬细胞炎性蛋白-2的肺水平没有降低。总之，这些发现表明HMG-1是急性炎性肺损伤的远端介质。
Acute inflammatory lung injury is often a delayed complication of critical illness and is associated with increased mortality, High mobility group-1 (HMG-1) protein, in addition to its role as a transcriptional regulatory factor, has recently been identified as a late mediator of endotoxin lethality. In the present studies, HMG-I given intratracheally produced acute inflammatory Injury to the lungs, with neutrophil accumulation, the development of lung edema, and increased pulmonary production of IL-1 beta, TNF-alpha, and macrophage-inflammatory protein-2, In endotoxin-induced acute lung inflammation, administration of anti-HMG-l Abs either before or after endotoxin exposure decreased the migration of neutrophils to the lungs as well as lung edema. These protective effects of anti-HMG-1 were specific, because pulmonary levels of IL-1 beta, TNF-alpha, or macrophage-inflammatory protein-2 were not decreased after therapy with anti-HMG-l, Together, these findings indicate that HMG-1 is a distal mediator of acute inflammatory lung injury.