Chignard M, Balloy V
Unité de Pharmacologie Cellulaire, Unité Institut National de la Santé et de la Recherche Médicale/Pasteur 485, Institut Pasteur, 75015 Paris, France.
Am J Physiol Lung Cell Mol Physiol. 2000 Dec;279(6):L1083-90. doi: 10.1152/ajplung.2000.279.6.L1083.
The intranasal administration of lipopolysaccharide (LPS) to mice triggers a huge influx of polymorphonuclear neutrophils (PMNs) into the airway spaces, with a peak at 48 h. The increase in protein concentration, an index of microvascular permeability, displayed a different pattern, i.e., a first increase with a plateau between 3 and 24 h followed by a second increase peaking at 72 h. When mice were depleted of circulating PMNs, the increase in protein concentration was inhibited at 3 h but not at 24 h. The lack of PMN involvement at 24 h was confirmed by 1) in situ activation of exudated PMNs present in the air spaces on intranasal administration of LPS and 2) induction of the migration of PMNs sequestered in lung vessels on intraperitoneal administration of LPS. These findings show that the increase in microvascular permeability during lung inflammation is due to at least two distinct mechanisms, an early one related to the neutrophil influx and a delayed one occurring even under neutropenic conditions.
给小鼠鼻内注射脂多糖（LPS）会引发大量多形核中性粒细胞（PMN）涌入气道间隙，在48小时达到峰值。蛋白质浓度的增加作为微血管通透性的指标，呈现出不同的模式，即先在3至24小时内升高并达到平台期，随后在72小时再次升高并达到峰值。当小鼠循环中的PMN被清除后，蛋白质浓度在3小时时的升高受到抑制，但在24小时时未受抑制。24小时时PMN未参与这一点通过以下两点得到证实：1）鼻内注射LPS后气道间隙中渗出的PMN的原位激活；2）腹腔注射LPS后肺血管中滞留的PMN的迁移诱导。这些发现表明，肺部炎症期间微血管通透性的增加至少归因于两种不同机制，一种早期机制与中性粒细胞的涌入有关，另一种延迟机制即使在中性粒细胞减少的情况下也会发生。
