Diesel exhaust particles (DEP) and their ultrafine fraction (UFP) are known to induce cardiovascular effects in exposed subjects. The mechanisms leading to these outcomes are still under investigation, but the activation of respiratory endothelium is likely to be involved. Particles translocation through the air-blood barrier and the release of mediators from the exposed epithelium have been suggested to participate in the process. Here we used a conditioned media in vitro model to investigate the role of epithelial-released mediators in the endothelial cells activation.

Diesel UFP were sampled from a Euro 4 vehicle run over a chassis dyno and lung epithelial BEAS-2B cells were exposed for 20 h (dose 5 μg/cm²). The exposure media were collected and used for endothelial HPMEC-ST1.6R cells treatment for 24 h. The processes related to oxidative stress and inflammation were investigated in the epithelial cells, accordingly to the present knowledge on DEP toxicity. The release of IL-6 and VEGF was significantly augmented in diesel exposed cells. In endothelial cells, VCAM-1 and ICAM-1 adhesion molecules levels were increased after exposure to the conditioned media. By interfering with IL-6 binding to its endothelial receptor, we demonstrate the role of this interleukin in inducing the endothelial response.

已知柴油机废气颗粒（DEP）及其超细级分（UFP）会在暴露的受试者中诱发心血管作用。导致这些结果的机制仍在研究中，但可能涉及呼吸道内皮的激活。已经建议颗粒通过气血屏障易位以及从暴露的上皮中释放介体参与该过程。在这里，我们使用条件培养基体外模型来研究上皮释放的介体在内皮细胞激活中的作用。

从在底盘测功机上行驶的Euro 4车辆采样柴油UFP，并将肺上皮BEAS-2B细胞暴露20小时（剂量5μg/ cm ²）。收集暴露介质并用于内皮HPMEC-ST1.6R细胞处理24小时。根据目前对DEP毒性的认识，在上皮细胞中研究了与氧化应激和炎症相关的过程。在暴露于柴油的细胞中，IL-6和VEGF的释放显着增加。在内皮细胞中，暴露于条件培养基后，VCAM-1和ICAM-1粘附分子水平增加。通过干扰IL-6与其内皮受体的结合，我们证明了这种白介素在诱导内皮反应中的作用。