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

Bengalli, R., Longhin, E., Marchetti, S., Proverbio, M., Battaglia, C., Camatini, M. (2017). The role of IL-6 released from pulmonary epithelial cells in diesel UFP-induced endothelial activation. ENVIRONMENTAL POLLUTION, 231, 1314-1321 [10.1016/j.envpol.2017.08.104].

The role of IL-6 released from pulmonary epithelial cells in diesel UFP-induced endothelial activation

BENGALLI, ROSSELLA DANIELA
Primo
;
LONGHIN, ELEONORA MARTA
Secondo
;
MARCHETTI, SARA;CAMATINI, MARINA CARLA
Ultimo
2017

Abstract

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
Articolo in rivista - Articolo scientifico
Conditioned media; Diesel ultrafine particles; Endothelial activation; IL-6; Inflammation; Toxicology; Pollution; Health, Toxicology and Mutagenesis
English
1314
1321
8
Bengalli, R., Longhin, E., Marchetti, S., Proverbio, M., Battaglia, C., Camatini, M. (2017). The role of IL-6 released from pulmonary epithelial cells in diesel UFP-induced endothelial activation. ENVIRONMENTAL POLLUTION, 231, 1314-1321 [10.1016/j.envpol.2017.08.104].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/170873
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