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Inhalation of ultrafine carbon particles triggers biphasic pro-inflammatory response in the mouse lung.
Eur. Respir. J. 28, 275-285 (2006)
High levels of particulate matter in ambient air are associated with increased respiratory and cardiovascular health problems. It has been hypothesised that it is the ultrafine particle fraction (diameter <100 nm) that is largely responsible for these effects. To evaluate the associated mechanisms on a molecular level, the current authors applied an expression profiling approach.
Healthy mice were exposed to either ultrafine carbon particles (UFCPs; mass concentration 380 µg·m-3) or filtered air for 4 and 24 h. Histology of the lungs did not indicate any pathomorphological changes after inhalation.
Examination of the bronchoalveolar lavage fluid revealed a small increase in polymorphonuclear cell number (ranging 0.6–1%) after UFCP inhalation, compared with clean air controls, suggesting a minor inflammatory response. However, DNA microarray profile analysis revealed a clearly biphasic response to particle exposure. After 4 h of inhalation, mainly heat shock proteins were induced, whereas after 24 h, different immunomodulatory proteins (osteopontin, galectin-3 and lipocalin-2) were upregulated in alveolar macrophages and septal cells.
In conclusion, these data indicate that inhalation of ultrafine carbon particles triggers a biphasic pro-inflammatory process in the lung, involving the activation of macrophages and the upregulation of immunomodulatory proteins.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
air pollution; alveolar macrophages; cytokine; expression profiling
ISSN (print) / ISBN
0903-1936
e-ISSN
1399-3003
Journal
European Respiratory Journal
Quellenangaben
Volume: 28,
Issue: 2,
Pages: 275-285
Publisher
European Respiratory Society
Publishing Place
Sheffield
Reviewing status
Peer reviewed
Institute(s)
Institute of Epidemiology (EPI)
Institute of Lung Health and Immunity (LHI)
Institute of Lung Health and Immunity (LHI)