Bayram H, Devalia J L, Sapsford R J, Ohtoshi T, Miyabara Y, Sagai M, Davies R J
Academic Department of Respiratory Medicine, St. Bartholomew's and the Royal London School of Medicine and Dentistry, The London Chest Hospital, London, United Kingdom.
Am J Respir Cell Mol Biol. 1998 Mar;18(3):441-8. doi: 10.1165/ajrcmb.18.3.2882.
Animal studies have reported that diesel exhaust particles (DEP), which constitute an important fraction of particulate air pollution, lead to inflammation and/or damage of the airways. To investigate the mechanisms underlying DEP-induced airway disease in humans, we have cultured human bronchial epithelial cells (HBEC) from surgically obtained bronchial explants and investigated the effects of purified DEP on the permeability and ciliary beat frequency (CBF) of HBEC, and on the release of inflammatory mediators from these cells. Exposure to 10-100 microg/ml DEP and a filtered solution of 50 microg/ml DEP significantly increased the electrical resistance of the cultures, reaching a maximum of 200% over baseline after 6 h incubation with 100 microg/ml DEP. In contrast, movement of 14C-labeled bovine serum albumin across cell cultures was not significantly altered by incubation of HBEC with DEP. Exposure to 50 microg/ml DEP, filtered DEP solution, and 100 migrog/ml DEP significantly attenuated the CBF of these cells by 51%, 33%, and 73%, respectively, from baseline after 24 h incubation. Similarly, 50 microg/ml DEP, filtered DEP solution, and 100 microg/ml DEP significantly increased the release of interleukin-8 from 12.9 pg/microg cellular protein to 41.6, 114.9, and 44.3 pg/microg cellular protein, respectively, after 24 h incubation. The release of granulocyte-macrophage colony stimulating factor (GM-CSF) and soluble intercellular adhesion molecule-1 (sICAM-1) was also significantly increased after exposure for 24 h to 50 microg/ml DEP (GM-CSF from 0.033 pg/microg cellular protein to 0.056 pg/mug cellular protein and sICAM-1 from 7.2 pg/microg cellular protein to 12.5 pg/microg cellular protein). These results suggest that exposure of HBEC to DEP may lead to adverse functional changes and release of proinflammatory mediators from these cells, and that these effects may influence the development of airway disease.
动物研究报告称，构成空气颗粒物污染重要部分的柴油废气颗粒（DEP）会导致气道炎症和/或损伤。为了研究DEP诱发人类气道疾病的潜在机制，我们从手术获取的支气管外植体中培养了人支气管上皮细胞（HBEC），并研究了纯化的DEP对HBEC通透性、纤毛摆动频率（CBF）以及这些细胞炎性介质释放的影响。暴露于10 - 100微克/毫升的DEP以及50微克/毫升的DEP过滤溶液后，培养物的电阻显著增加，在与100微克/毫升DEP孵育6小时后，比基线最高增加了200%。相比之下，用DEP孵育HBEC并未显著改变14C标记的牛血清白蛋白在细胞培养物中的移动情况。暴露于50微克/毫升DEP、过滤后的DEP溶液以及100微克/毫升DEP后，孵育24小时后，这些细胞的CBF分别比基线显著降低了51%、33%和73%。同样，孵育24小时后，50微克/毫升DEP、过滤后的DEP溶液以及100微克/毫升DEP分别使白细胞介素-8的释放量从12.9皮克/微克细胞蛋白显著增加至41.6、114.9和44.3皮克/微克细胞蛋白。暴露于50微克/毫升DEP 24小时后，粒细胞-巨噬细胞集落刺激因子（GM-CSF）和可溶性细胞间黏附分子-1（sICAM-1）的释放也显著增加（GM-CSF从0.033皮克/微克细胞蛋白增加至0.056皮克/微克细胞蛋白，sICAM-1从7.2皮克/微克细胞蛋白增加至12.5皮克/微克细胞蛋白）。这些结果表明，HBEC暴露于DEP可能导致这些细胞出现不良功能变化并释放促炎介质，且这些影响可能会影响气道疾病的发展。
