Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Professor Robert Barouki, University of Paris Descartes School of Medicine, France
- Second opponent: Professor Asbjørn Magne Nilsen, Norwegian University of Science and Technology
- Third member and chair of the evaluation committee: Associate Professor May Brit Samersaw-Lund, University of Oslo
Chair of the Defence
Professor II Johny Kongerud, Faculty of Medicine, University of Oslo
Principal Supervisor
Department Director Johan Øvrevik, Norwegian Institute of Public Health
Summary
Air pollution, especially combustion-derived particles, are known to contribute to development of cardiovascular disease. How this occurs, the cellular mechanisms involved and what components of particulate matter that triggers these effects, is still debated.
We found that lipophilic organic chemicals (OC) from diesel exhaust particles (DEP) have pro-inflammatory effects in bronchial epithelial and endothelial cells. Furthermore, soluble lipophilic chemicals seemed to penetrate the alveolar layer of a 3D-triculture mimicking the alveolar barrier and induce inflammation-associated and aryl hydrocarbon receptor (AhR) regulated genes in the endothelial cell-layer. AhR, protease activated receptor 2 (PAR-2), β-adrenergic receptors (βARs) and oxidative stress were involved in these effects.
We also found that lipophilic OC from DEP triggered store operated and receptor operated calcium entry in endothelial cells via AhR non-genomic signaling. Furthermore, membrane re-shuffling, PAR-2 and β-adrenergic receptors (βARs) were involved in these responses. Finally, the calcium effects and inflammatory responses seemed partially interrelated.
Elucidating what components of air pollution cause adverse health effects, and through what mechanisms this occurs, may have implications for risk assessment as well as future combustion and cleansing technology.
Additional information
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