PT  - JOURNAL ARTICLE
AU  - E. André
AU  - T. Stoeger
AU  - S. Takenaka
AU  - M. Bahnweg
AU  - B. Ritter
AU  - E. Karg
AU  - B. Lentner
AU  - C. Reinhard
AU  - H. Schulz
AU  - M. Wjst
TI  - Inhalation of ultrafine carbon particles triggers biphasic pro-inflammatory response in the mouse lung
AID  - 10.1183/09031936.06.00071205
DP  - 2006 Aug 01
TA  - European Respiratory Journal
PG  - 275--285
VI  - 28
IP  - 2
4099  - http://erj.ersjournals.com/content/28/2/275.short
4100  - http://erj.ersjournals.com/content/28/2/275.full
SO  - Eur Respir J2006 Aug 01; 28
AB  - 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.