Ultrafine particles from diesel vehicle emissions at different driving cycles induce differential vascular pro-inflammatory responses: Implication of chemical components and NF-κB signaling

UFP2 contained a higher level of redox active organic compounds and metals on a per PM mass basis than UFP1. While both UFP1 and UFP2 induced superoxide production and up-regulated stress response genes such as heme oxygenease-1 (HO-1), OKL38, and tissue factor (TF), only UFP2 induced the expression of pro-inflammatory genes such as IL-8 (2.8 ± 0.3-fold), MCP-1 (3.9 ± 0.4-fold), and VCAM (6.5 ± 1.1-fold) (n = 3, P < 0.05). UFP2-exposed HAEC also bound to a higher number of monocytes than UFP1-exposed HAEC (Control = 70 ± 7.5, UFP1 = 106.7 ± 12.5, UFP2 = 137.0 ± 8.0, n = 3, P < 0.05). Adenovirus NF-κB Luciferase reporter assays revealed that UFP2, but not UFP1, significantly induced NF-κB activities. NF-κB inhibitor, CAY10512, significantly abrogated UFP2-induced pro-inflammatory gene expression and monocyte binding.While UFP1 induced higher level of oxidative stress and stress response gene expression, only UFP2, with higher levels of redox active organic compounds and metals, induced pro-inflammatory responses via NF-κB signaling. Thus, UFP with distinct chemical compositions caused differential response patterns in endothelial cells.Exposure to atmospheric particulate matter (PM) is associated with cardiovascular and respiratory diseases [1,2]. Diesel and gasoline vehicle emissions in the urban areas have dominant contributions to ambient particles, especially those in the ultrafine range (Dp < 100 nm). Because of their small size and large surface area per unit mass, ultrafine particles (UFP) have demonstrated unique biochemical characteristics, such as enhanced ability to adsorb or absorb organic molecules and to penetrate cellular targets in the human pulmonary and cardiovascular system [3-5]. Inhaled nano-sized particles in air pollutant can transmigrate across human pulmonary epithelium into systemic arterial circulation [6-8]. Circulating nano-sized particles may deposit at so-called hot spots such as artery bifurcations and accumulated to high concentration