Boland S, Baeza-Squiban A, Fournier T, Houcine O, Gendron M C, Chévrier M, Jouvenot G, Coste A, Aubier M, Marano F
Laboratoire de Cytophysiologie et Toxicologie Cellulaire, Institut J. Monod, Université Paris VII Denis Diderot, 75251 Paris, France. p2
Am J Physiol. 1999 Apr;276(4):L604-13. doi: 10.1152/ajplung.1999.276.4.L604.
The involvement of diesel exhaust particles (DEPs) in respiratory diseases was evaluated by studying their effects on two in vitro models of human airway epithelial cells. The cytotoxicity of DEPs, their phagocytosis, and the resulting immune response were investigated in a human bronchial epithelial cell line (16HBE14o-) as well as in human nasal epithelial cells in primary culture. DEP exposure induced a time- and dose-dependent membrane damage. Transmission electron microscopy showed that DEPs underwent endocytosis by epithelial cells and translocated through the epithelial cell sheet. Flow cytometric measurements allowed establishment of the time and dose dependency of this phagocytosis and its nonspecificity with different particles (DEPs, carbon black, and latex particles). DEPs also induced a time-dependent increase in interleukin-8, granulocyte-macrophage colony-stimulating factor, and interleukin-1beta release. This inflammatory response occurred later than phagocytosis, and its extent seems to depend on the content of adsorbed organic compounds because carbon black had no effect on cytokine release. Furthermore, exhaust gas posttreatments, which diminished the adsorbed organic compounds, reduced the DEP-induced increase in granulocyte-macrophage colony-stimulating factor release. These results suggest that DEPs could 1) be phagocytosed by airway epithelial cells and 2) induce a specific inflammatory response.
通过研究柴油尾气颗粒(DEPs)对两种人呼吸道上皮细胞体外模型的影响,评估了其在呼吸道疾病中的作用。在人支气管上皮细胞系(16HBE14o-)以及原代培养的人鼻上皮细胞中,研究了DEPs的细胞毒性、吞噬作用及由此产生的免疫反应。DEP暴露诱导了时间和剂量依赖性的膜损伤。透射电子显微镜显示,DEPs被上皮细胞内吞,并穿过上皮细胞层。流式细胞术测量确定了这种吞噬作用的时间和剂量依赖性及其对不同颗粒(DEPs、炭黑和乳胶颗粒)的非特异性。DEPs还诱导白细胞介素-8、粒细胞-巨噬细胞集落刺激因子和白细胞介素-1β释放随时间增加。这种炎症反应比吞噬作用发生得晚,其程度似乎取决于吸附有机化合物的含量,因为炭黑对细胞因子释放没有影响。此外,减少吸附有机化合物的废气后处理降低了DEP诱导的粒细胞-巨噬细胞集落刺激因子释放增加。这些结果表明,DEPs可能1)被气道上皮细胞吞噬,2)诱导特异性炎症反应。