Lipophilic components of diesel exhaust particles induce pro-inflammatory responses in human endothelial cells through AhR dependent pathway(s).

ABSTRACT:

Background

Exposure to traffic-derived particulate matter (PM), such as diesel exhaust particles (DEP), is a leading environmental cause of cardiovascular disease (CVD), and may contribute to endothelial dysfunction and development of atherosclerosis. It is still debated how DEP and other inhaled PM can contribute to CVD. However, organic chemicals (OC) adhered to the particle surface, are considered central to many of the biological effects. In the present study, we have explored the ability of OC from DEP to reach the endothelium and trigger pro-inflammatory reactions, a central step on the path to atherosclerosis.

Results

Exposure-relevant concentrations of DEP (0.12 μg/cm²) applied on the epithelial side of an alveolar 3D tri-culture, rapidly induced pro-infla

SUBMITTER: Brinchmann BC 

PROVIDER: S-EPMC5948689 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature