Choe N, Zhang J, Iwagaki A, Tanaka S, Hemenway D R, Kagan E
Department of Pathology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799, USA.
Am J Physiol. 1999 Aug;277(2):L292-300. doi: 10.1152/ajplung.1999.277.2.L292.
This study was designed to assess the effects of in vitro and in vivo asbestos exposure on the adhesion of rat pleural leukocytes (RPLs) labeled with the fluorochrome calcein AM to rat pleural mesothelial cells (RPMCs). Exposure of RPMCs for 24 h to either crocidolite or chrysotile fibers (1.25-10 microgram/cm(2)) increased the adhesion of RPLs to RPMCs in a dose-dependent fashion, an effect that was potentiated by interleukin-1beta. These findings were not observed with nonfibrogenic carbonyl iron particles. Crocidolite and chrysotile plus interleukin-1beta also upregulated vascular cell adhesion molecule-1 mRNA and protein expression in RPMCs, and the binding of RPL to asbestos-treated RPMCs was abrogated by anti-vascular cell adhesion molecule-1 antibody. PRLs exposed by intermittent inhalation to crocidolite for 2 wk manifested significantly greater binding to RPMCs than did RPLs from sham-exposed animals. The ability of asbestos fibers to upregulate RPL adhesion to RPMCs may play a role in the induction and/or potentiation of asbestos-induced pleural injury.
本研究旨在评估体外和体内石棉暴露对用荧光染料钙黄绿素乙酰甲酯标记的大鼠胸膜白细胞(RPLs)与大鼠胸膜间皮细胞(RPMCs)黏附的影响。将RPMCs暴露于青石棉或温石棉纤维(1.25 - 10微克/平方厘米)24小时,会以剂量依赖的方式增加RPLs与RPMCs的黏附,白细胞介素-1β可增强这种效应。非致纤维化的羰基铁颗粒未观察到这些结果。青石棉和温石棉加白细胞介素-1β也上调了RPMCs中血管细胞黏附分子-1的mRNA和蛋白表达,抗血管细胞黏附分子-1抗体可消除RPL与经石棉处理的RPMCs的结合。通过间歇吸入暴露于青石棉2周的PRLs与假暴露动物的RPLs相比,与RPMCs的结合明显更强。石棉纤维上调RPL与RPMCs黏附的能力可能在石棉诱导的胸膜损伤的诱导和/或增强中起作用。