Migratory responses of PMN after intraperitoneal and intratracheal administration of lipopolysaccharide
Migratory responses of PMN after intraperitoneal and intratracheal administration of lipopolysaccharide
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DOI：
10.1152/ajplung.1996.270.5.l836
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发表时间：
1996-05-01
影响因子：
4.9
通讯作者：
Hirano, S
中科院分区：
文献类型：
--
作者：
Hirano, S
本实验主要观察了腹腔注射脂多糖（LPS）后小鼠肺血管内多形核白细胞（PMN）的聚集及PMN对LPS的迁移反应。腹腔注射的LPS被迅速吸收到血液中，循环LPS浓度在注射后1h达到峰值。血中肿瘤坏死因子浓度于注射后0.5h开始升高，1h达高峰。腹腔注射后0.5 h，肺血管相关PMN数量增加7.5倍。肺组织中未见中性粒细胞渗出和损伤，而肝组织中可见混合细胞浸润。虽然腹腔内注射LPS导致肺血管内的一个显着的PMN积累，腹腔内注射LPS显着和剂量依赖性地取消了LPS诱导的PMN浸润和明显的血浆蛋白泄漏到肺泡腔。另一方面，腹膜前灌注LPS增强而不是减少腹腔内LPS诱导的PMN浸润到腹腔。在大鼠中，亚致死剂量的腹腔注射LPS引起肺泡PMN的适度增加，但减少intraperheal LPS诱导的强大的transulphanum PMN浸润。虽然肺血管相关PMN不同迁移反应的机制尚不清楚，但腹腔注射LPS对经肺PMN浸润的抑制作用可能适用于脓毒性肺疾病的治疗。
The present study was undertaken primarily to investigate accumulation of polymorphonuclear leukocytes (PMN) within the lung vasculature after intraperitoneal injection of lipopolysaccharide (LPS) and migratory responses of those intravascular PMN to intratracheally instilled LPS in mice. Intraperitoneally injected LPS was absorbed into the blood rapidly, and the concentration of circulating LPS peaked at 1 h postinjection. Tumor necrosis factor concentration in blood began to increase at 0.5 h and also peaked at 1 h postinjection. The number of lung vascular-associated PMN was increased 7.5-fold at 0.5 h post-intraperitoneal injection. However, neither diapedesis of PMN nor injury was observed in the lung, while mixed cell infiltration was observed in the liver. Although intraperitoneally injected LPS caused a significant PMN accumulation within the lung vasculature, pre-intraperitoneal injection of LPS dramatically and dose dependently abolished both intratracheal LPS-inducible PMN infiltration and apparent plasma protein leakage into the alveolar space. On the other hand, pre-intratracheal instillation of LPS enhanced rather than reduced intraperitoneal LPS-inducible PMN infiltration into the peritoneal cavity. In rats, a sublethal dose of intraperitoneally injected LPS caused a modest increase in alveolar PMN and yet reduced intratracheal LPS-inducible robust transpulmonary PMN infiltration. Although mechanisms of different migratory responses of the lung vasculature-associated PMN are unknown, the inhibitory effects of intraperitoneally injected LPS on transpulmonary PMN infiltration may be applicable to treatments for septic lung diseases.