ICAM-1 expression and its role in cigarette smoke inhalationinduced lung inflammation in the mouse.

吸烟可导致外周肺内中性粒细胞(PMN)和单个核细胞聚集。本研究旨在探讨细胞间黏附分子-1(ICAM-1)在急性香烟烟雾吸入致小鼠肺部炎症中的作用。ICR小鼠暴露于100支香烟中，用抗ICAM-1单抗(ICAM-mAb+烟雾组)磷酸盐缓冲盐水(烟雾组)处理2 h。吸烟组大鼠吸入香烟后12h，肺泡灌洗液中细胞总数、巨噬细胞数和中性粒细胞数均显著增加。用抗ICAM-1单抗(P&lt；O01)预处理后，这种炎性细胞的聚集显著减少。髓过氧化物酶阳性的PMN与血管内皮细胞和细支气管上皮的粘附率在暴露后12h显著增加，经抗ICAM-1单抗处理后，这种粘附性明显减弱(p&lt；0.05)。染毒后细支气管壁上皮细胞ICAM-1表达增强。提示ICAM-1的表达上调可能在香烟烟雾吸入所致的呼吸道炎症过程中起重要作用。

Cigarette smoking induces accumulation of polymorphonuclear leukocytes (PMNs) and mononuclear cells in the peripheral lung. The purpose of this report was to investigate the role of intercellular adhesion molecule-1 (ICAM-1) in a murine model of acute cigarette smoke inhalation-induced lung inflammation. ICR mice were exposed to 100 cigarettes for 2 h pretreated with phosphate buffered saline (Smoke group), an anti-ICAM-1 mAb (ICAMmAb+Smoke group). In the Smoke group, significant increases in total cell, macrophage and PMN counts of bronchoalveolar lavage fluid were observed at 12 h after cigarette smoke exposure. This accumulation of inflammatory cells was significantly reduced by the pretreatment with an anti-ICAM-1 mAb (p<O.O1). Adherence of myeloperoxydase positive PMNs to vascular endothelium and bronchiolar epithelium significantly increased at 12 h after exposure, and this increase of adherent PMNs was attenuated significantly by the pretreatment with anti-ICAM-1 mAb (p<O.O5). The increased expression of ICAM-1 on bronchiolar epithelium was observed after exposure. These observations suggest that the upregulation of ICAM-1 may play an important role in the inflammatory process of airways caused by cigarette smoke inhalation.